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Neuroscience - Unit 5 > Section 3 > Flashcards

Section 3 Flashcards

1
Q

What is the function of the thalamus?

A

it is the gateway to the cerebral cortex, and specific systems end in particular regions of the thalamus (thalamic nuclei) prior to projecting to specific regions of the cortex.

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2
Q

Primary visual cortex is

A

area 17

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3
Q

Primary somatosensory cortex is

A

made up of areas 3, 1, and 2

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4
Q

Primary motor cortex is

A

area 4

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5
Q

Premotor is

A

area 6

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6
Q

Auditory cortices are

A

areas 41, and 42

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7
Q

What is the relationship between the basal ganglia, cerebellum and the thalamus?

A

Motor information from the basal ganglia and cerebellum also send projections to specific thalamic nuclei, which in turn project to motor areas of the cortex.

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8
Q

The lateral geniculate nucleus

A

receives input from the optic tract, and projects to the primary visual cortex (V1 or Brodmann area 17).

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9
Q

The medial geniculate nucleus

A

receives auditory input from the inferior colliculus, an auditory relay nucleus, via the brachium of the inferior colliculus, and projects to the auditory cortex (A1 or areas 41).

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10
Q

The anterior tubercle consists of what?

A

mainly of the anterior nucleus, which receives input from the mammillary bodies (hypothalamus) and projects to the cingulate gyrus.

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11
Q

Each area of cortex that receives a projection from a specific thalamic nucleus

A

also sends a projection back to that nucleus. Although only some of these nuclei have clinical significance (i.e., pathology is common and causes visible symptoms)

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12
Q

transmitting auditory information

A

vestibulocochlear nerve, primary auditory cortex, medial geniculate body, inferior colliculus and brachium of the inferior colliculus

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13
Q

What is the location of the anterior nucleus (A)?

A

anterior tubercle

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14
Q

What is the input for the anterior nucleus (A)?

A

mammillary bodies

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15
Q

What is the target for the anterior nucleus (A)?

A

cingulated gyrus

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16
Q

What is the function of the anterior nucleus (A)?

A

emotions

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17
Q

What is the location of the dorsomedial nucleus (DM) or mediodorsal nucleus?

A

Medial to internal medullary lamina

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18
Q

What is the input for the dorsomedial nucleus (DM) or mediodorsal nucleus?

A

1) amygdala 2) hypothalamus 3) spinal trigeminal nucleus 4) ALS

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19
Q

What is the target for the dorsomedial nucleus (DM) or mediodorsal nucleus?

A

Frontal lobe anterior to motor areas and to orbital cortex

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20
Q

What is the function of the dorsomedial nucleus (DM) or mediodorsal nucleus?

A

Emotions and non motor frontal lobe functions

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21
Q

What is the location of the ventral anterior (VA) nucleus?

A

Lateral to internal medullary lamina

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22
Q

What is the input for the ventral anterior (VA) nucleus?

A

1) globus pallidus 2) cerebellum

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23
Q

What is the target for the ventral anterior (VA) nucleus?

A

premotor cortex

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24
Q

What is the function of the ventral anterior (VA) nucleus?

A

motor

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25
Q

What is the location of the ventral lateral (VL) nucleus?

A

Posterior to ventral anterior (VA) nucleus

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26
Q

What is the input for the ventral lateral (VL) nucleus?

A

1) globus pallidus 2) cerebellum

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27
Q

What is the target for the ventral lateral (VL) nucleus?

A

1) precentral gyrus 2) premotor cortex

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28
Q

What is the function of the ventral lateral (VL) nucleus?

A

motor

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29
Q

What is the location of the ventral posterolateral nucleus (VPL)?

A

Posterior to VL nucleus

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30
Q

What is the input for the ventral posterolateral nucleus (VPL)?

A

Medial lemniscus (Dorsal Column Nuclei)

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31
Q

What is the target for the ventral posterolateral nucleus (VPL)?

A

Postcentral gyrus

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32
Q

What is the function of the ventral posterolateral nucleus (VPL)?

A

Somatic sensation, body

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33
Q

What is the location of the ventral posteromedial nucleus (VPM)?

A

Medial to VPL

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34
Q

What is the input for the ventral posteromedial nucleus (VPM)?

A

Medial lemniscus (Trigeminal Sensory Nuclei)

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35
Q

What is the target for the ventral posteromedial nucleus (VPM)?

A

Postcentral gyrus (near lateral fissure)

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36
Q

What is the function of the ventral posteromedial nucleus (VPM)?

A

Somatic sensation, head

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37
Q

What is the location of the pulvinar (P)?

A

posterior thalamus

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38
Q

What is the input for the pulvinar (P)?

A

1) superior colliculus 2) occipital lobe 3) temporal lobe 4) parietal lobe

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39
Q

What is the target for the pulvinar (P)?

A

occipital lobe, temporal lobe, parietal lobe

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40
Q

What is the function of the pulvinar (P)?

A

1) visual perception 2) language

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41
Q

What is the location of the medial geniculate nucleus (MGN)?

A

Posterior ventral surface of thalamus

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42
Q

What is the input for the medial geniculate nucleus (MGN)?

A

Inferior colliculus

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43
Q

What is the target for the medial geniculate nucleus (MGN)?

A

Auditory cortex

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44
Q

What is the function of the medial geniculate nucleus (MGN)?

A

audition

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45
Q

What is the location of the lateral geniculate nucleus (LGN)?

A

Posterior ventral surface of thalamus

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46
Q

What is the input for the lateral geniculate nucleus (LGN)?

A

Optic tract

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47
Q

What is the target for the lateral geniculate nucleus (LGN)?

A

Visual cortex

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48
Q

What is the function of the lateral geniculate nucleus (LGN)?

A

vision

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49
Q

What is the location of the intralaminar nucleus (ILN)?

A

Embedded in internal medullary lamina

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50
Q

What is the input for the intralaminar nucleus (ILN)?

A

1) Reticular formation 2) spinal cord 3) spinal trigeminal nucleus 4) ALS 5) globus pallidus

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51
Q

What is the target for the intralaminar nucleus (ILN)?

A

Basal ganglia, diffusely to cortex

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52
Q

What is the function of the intralaminar nucleus (ILN)?

A

Attention, arousal

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53
Q

What does the lemniscal system carry?

A

Epicritic sense (from trunk and limbs)

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54
Q

What does epicritic sense mean?

A

Vibration, tactile form (2 point discrimination) position sense simple touch

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55
Q

What does the anterolateral (spinothalamic) carry?

A

Protopathic sense (from trunk and limbs)

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56
Q

What does protopathic sense mean?

A

Pain, temperature sense and simple touch

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57
Q

What does spino-cerebellar carries?

A

Proprioceptive (from trunk & limbs)

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58
Q

What does proprioceptive mean?

A

Muscle, joint information

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59
Q

What does the trigeminal system carry?

A

All sensation (from head and neck)

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60
Q

What does it mean that the trigeminal system mean by carrying all sensation?

A

1) epicritic 2) protopathic 3) proprioceptive

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61
Q

In the lemniscal system information comes to the spinal cord via

A

large-diameter dorsal root axons.

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62
Q

In the lemniscal system large neurons are especially vulnerable to what?

A

insult from ischemia, toxicity, bacteria, etc,

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63
Q

In the lemniscal system early symptoms of peripheral nerve disease often first show as what?

A

“epicritic” rather than “protopathic” losses

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64
Q

In the lemniscal system dorsal root axons from the lower trunk and limbs enter where?

A

at lower thoracic and lumbosacral levels, send a segmental collateral to the dorsal gray matter, and ascend the cord as the gracile fasciculus.

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65
Q

In the lemniscal system gracile fasciculus

A

it’s a segmental collateral to the dorsal grey matter and ascends the cord from the lower thoracic and lumbosacral levels

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66
Q

In the lemniscal system upper trunk and limb axons enter where?

A

at upper thoracic and cervical levels and ascend as the cuneate fasciculus.

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67
Q

In the lemniscal system, what does the cuneate fasciculus do?

A

ascends the cord from the upper thoracic and cervical levels

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68
Q

What would damage to the cuneate or gracile fasciculus on one side cause and why?

A

Damage e.g. on the left, would cause epicritic losses on the same (left) side of the body because these fasciculi ascend the cord on the same side as the body they serve

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69
Q

In the lemniscal system where do the fasciculi (axons) synapse (end)?

A

in the medulla

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70
Q

In the lemniscal system what happens to the information after it synapses in the medulla?

A

it is picked up by second-order neurons whose cell bodies lie in the gracile & cuneate nuclei

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71
Q

In the lemniscal system what happens to the information from the fascicule after the gracile and cuneate nuclei?

A

Axons of these cells exit the nuclei, cross to the other side in the medulla (called “internal arcuate fibers”), at which time they are renamed the medial lemniscus

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72
Q

In the lemniscal system what happens to the information from the fascicule after the medial leminscus?

A

The medial lemniscus ascends to the thalamus

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73
Q

In the lemniscal system damage to the right medial lemniscus would produce what, and why would you see these symptoms?

A

epicritic symptoms on the patient’s left side of the body because of the crossing

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74
Q

In the lemniscal system the medial lemniscus synapses in the

A

ventral posterolateral nucleus of the thalamus (VPL)

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75
Q

In the lemniscal system what happens to the information from the fascicule after it gets to the VPL?

A

it is then picked up by the third-order neurons, which carry it to the postcentral gyrus (aka S1, Brodmann’s area 3,2,1) via the internal capsule

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76
Q

pathology on the right side of the brain at the level of the postcentral gyrus would cause what?

A

symptoms on the left side of the body

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77
Q

In the lemniscal system, epicritic symptoms include the loss of

A

1) stereognosis 2) two-point tactile 3) position sense 4) vibration 5) simple touch

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78
Q

stereognosis:

A

cannot recognize tactile shapes placed in the hand (called astereognosis).

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79
Q

two-point tactile:

A

cannot separate the location of two simultaneous touches near each other on the skin

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80
Q

position sense:

A

cannot state the position of the limb, without visual cues. This has some motor consequences, causing a shuffling gait, and reaching inaccuracies

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81
Q

vibration:

A

insensitivity to high frequency stimulation, such as vibrations from a tuning fork

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82
Q

simple touch:

A

largely intact. The patient knows when she has been touched, but with slightly less sensitivity

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83
Q

In the anterolateral (or spinothalamic) system information comes to the spinal cord via what?

A

small-diameter dorsal root axons.

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84
Q

In the anterolateral (or spinothalamic) system information travel in a tract on the dorsolateral aspect of the spinal cord called and where do they synapse?

A

Lissauer’s tract or dorsolateral fasciculus up or down one or two spinal segments only and then synapse immediately in the dorsal horn of the spinal cord, i.e. at or near the level they enter.

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85
Q

After one or more synapses within local networks of the dorsal horn, axons carrying this information ascend in the white matter of the cord as the

A

anterolateral (AL, or spinothalamic) tract or system.

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86
Q

Most of the AL tract neurons first do what?

A

cross the midline before ascending to the brain.

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87
Q

Damage to the AL tract on one side will cause what?

A

protopathic symptoms on the opposite side of the body

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88
Q

AL axons synapse where?

A

diffusely and at every level in the brainstem.

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89
Q

Where do most of the AL axons terminate?

A

in the reticular formation

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90
Q

A few of the AL axons make it where?

A

Some make it to the thalamus where they terminate in; 1) VPL as well as several other nuclei including the 2) dorsomedial (DM or MD) and 3) intralaminar nuclei.

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91
Q

What happens to ascending axons from areas of the reticular formation?

A

receiving anterolateral projections relay this information to the same regions of the thalamus.

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92
Q

In the AL system, signals pass via the internal capsule to where?

A

primary somatosensory cortex (postcentral g. or SI, areas 3,1,2 of Brodmann) as well as to more widespread areas related to pain perception and appreciation (anterior cingulate, frontal lobe).

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93
Q

In the AL system, at every level, the symptoms of pathology are?

A

reduced protopathic sensation of the trunk and limbs on the opposite side of the body.

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94
Q

What does reduced “protopathic” mean?

A

1) pain 2) temperature 3) simple touch

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95
Q

In the AL system, reduced protopathic; pain?

A

reduced or no sense of pain from a pinprick or from chronic internal pain

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96
Q

In the AL system, reduced protopathic; temperature?

A

reduced or lost sense of warming and cooling of the skin

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97
Q

In the AL system, reduced protopathic; simple touch?

A

largely intact, but reduced in sensitivity

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98
Q

In the Spino-cerebellar system, where do the signals come from and where do they go?

A

Signals from muscle spindles and joint receptors enter the CNS via the dorsal roots, and after one or more synapses, spino-cerebellar tracts carry this information to the same side of the cerebellum.

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99
Q

In the Spino-cerebellar system does the information go to the same side or the opposite side of the cerebellum?

A

Same side

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100
Q

In the Spino-cerebellar system axons from the leg and lower trunk do what?

A

ascend as part of the gracile fasciculus.

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101
Q

These axons from the leg and lower trunk that ascend as part of the gracile fasciculus terminate where?

A

in the dorsal nucleus of Clarke or Clarke’s nucleus in the thoracic cord.

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102
Q

In the Spino-cerebellar system what happens to the information from the leg and lower trunk after Clarke’s nucleus?

A

Second order neurons from Clarke’s nucleus ascend to the cerebellum along the lateral rim of the white matter as the dorsal spinocerebellar tract.

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103
Q

In the Spino-cerebellar system what happens to the component from the arm and upper torso?

A

it ascends with the cuneate fasciculus to the medulla

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104
Q

In the Spino-cerebellar system where do the component from the arm and upper torso synapse?

A

in the accessory (or lateral) cuneate nucleus.

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105
Q

In the Spino-cerebellar system where does the component from the arm and upper torse synapse?

A

They synapse in the accessory (or lateral) cuneate nucleus.

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106
Q

In the Spino-cerebellar system what happens to the information from the arm and upper torso after they synapse in the accessory or lateral cuneate nucleus?

A

Second-order neurons carry the signals to the cerebellum as the cuneocerebellar tract.

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107
Q

In the Spino-cerebellar system is there crossing to the opposite side as the incoming information?

A

Several other pathways also carry information to the cerebellum, ending PRIMARILY ON THE SAME SIDE of the cerebellum, even though the anterior or ventral spinocerebellar tract crosses, like the anterolateral system, but then the majority re-crosses prior

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108
Q

Pathology of the Spino-cerebellar system.

A

The clinical effects of pathology of these tracts are seldom seen, since they are rarely damaged in isolation

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109
Q

In the Trigeminal System most somatosensory information from the head and neck enters the CNS via

A

CN 5 axons whose cell bodies are in the trigeminal ganglion. Some information also arrives via CN 7, 9 and 10.

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110
Q

Axons of the trigeminal nerve convey epicritic sensation synapse immediately where?

A

in the principal or chief sensory nucleus of CN 5 and in the pontine part of the spinal nucleus of CN 5.

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111
Q

In the trigeminal system what happens after epicritic sensation synapses in the principle or chief sensory nucleus of CN 5 and in the pontine part of the spinal nucleus of CN 5?

A

Second-order neurons leave these nuclei, cross the midline, and join the medial lemniscus en route to the thalamus (ventral posteromedial nucleus, VPM)

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112
Q

In the Trigeminal System what happens after the VPM of the thalamus?

A

Subsequent neurons forward the signals to the postcentral gyrus

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113
Q

In the trigeminal system, describe the projection between the VPM and the postcentral gyrus?

A

the projection of VPM is to the portion of the postcentral gyrus near the lateral fissure (face representation)

114
Q

Regarding the trigeminal system, describe the interaction between the VPL and the Postcentral gyrus.

A

There is a topograpahic representation of the rest of the body’s surface from VPL to the postcentral gyrus giving a sensory homunculus with the arm, body, and thigh represented in turn along the postcentral gyrus with the leg and foot on its medial surfac

115
Q

A homunculus is found in the motor cortex where?

A

the motor face representation again located near the lateral fissure

116
Q

In the Trigeminal System what does pathology of the pontine portion of the system cause?

A

epicritic losses of the head and neck.

117
Q

In the trigeminal system, are the symptoms associated with the pontine portion occur on the same or opposite side of the injury?

A

1) SAME SIDE = The symptoms are on the same side if the pathology lies before the crossing, i.e. in the trigeminal nerve or nuclei. 2) OPPOSITE SIDE = Pathology after the crossing, i.e. medial lemniscus, thalamus, cortex, will cause losses on the opposite

118
Q

In the trigeminal system what happens to axons from second portion of the trigeminal nerve conveying protopathic information?

A

they descend toward the spinal cord as the spinal tract of CN 5

119
Q

In the trigeminal system what happens to the axons carrying the protopathic information as they descend as the spinal tract of CN 5?

A

they synapse along the way in the adjacent caudal portion of the spinal nucleus of CN 5

120
Q

In the trigeminal system carrying protopathic information, what happens after it gets to the spinal nucleus?

A

Second-order neurons leave the caudal part of the spinal nucleus, cross the midline, and project largely to the reticular formation

121
Q

In the trigeminal system carrying protopathic information what happens to the axons from the areas of the reticular formation?

A

they project to VPM and other portions of the thalamus, including intralaminar nuclei traveling more diffusely than the epicritic portion but in the same general location in the pons and midbrain as the anterolateral tract.

122
Q

Pathology of the caudal portion of the spinal trigeminal tract (in medulla) and nucleus of CN5, cause what?

A

protopathic losses on the same side of the head.

123
Q

How can you selectively relieve intractable pain of the head and neck, without impairing epicritic sensation?

A

A surgical lesion of the spinal tract or nucleus in the medulla

124
Q

What location of pathology would affect the opposite side of the head (regarding the trigeminal system)?

A

Pathology after the crossing (i.e. from the reticular formation), particularly at a pontine or midbrain level

125
Q

In the trigeminal system, what else is carried in addition to carrying epicirtic and protopathic information?

A

proprioceptive input from the face

126
Q

What is the path for the axons in the trigeminal nerve carrying proprioceptive information?

A

These axons are continuous with the neurons of the mesencephalic nucleus of CN 5 (similar to trigeminal ganglion neurons, but located within the brain)

127
Q

What happens to the axons called the mesencephalic tract of CN 5?

A

They (carrying proprioceptive input from the face) continue through the mesencephalic nucleus of CN 5 to synapse with neurons of the motor nucleus of CN 5 for jaw reflexes, and via the reticular formation before projecting to the cerebellum.

128
Q

Where does the motor component of the trigeminal nerve arise from?

A

These axons arise from cells in the motor nucleus of CN 5 in the pons

129
Q

What does the motor component of the trigeminal nerve innervate?

A

the muscles of mastication on the same side.

130
Q

Pathology of the trigeminal nerve will do what?

A

both reduce facial sensation and weaken the jaw of the patient. The jaw may jut to the side of injury when opened.

131
Q

What are the two descending networks that carry motor commands to the brainstem and spinal cord?

A

1) Pyramidal – Direct cortical input system 2) Brainstem-spinal -indirect cortical control (sometimes called extrapyramidal)

132
Q

For the Pyramidal – Direct cortical input system what are the component tracts?

A

1) cortico-bulbar 2) cortico-pontine 3) cortico-rubro-olivary 4) cortico-spinal

133
Q

For the Pyramidal – Direct cortical input system what are the origin of tracts?

A

all areas of neocortex, esp. frontal and parietal lobes

134
Q

For the Pyramidal – Direct cortical input system what does it control?

A

cranial nerve nuclei cerebellum via pontine nuclei and a cortico-rubroolive circuit spinal motor neurons

135
Q

For the Brainstem-spinal -indirect cortical control system (sometimes called extrapyramidal), what are the component tracts?

A

1) Vestibulospinal 2) tectospinal 3) reticulospinal 4) rubrospinal

136
Q

For the Brainstem-spinal -indirect cortical control system (extrapyramidal), what are the origin of tracts?

A

1) vestibular nuclei 2) tectum 3) reticular formation 4) red nucleus

137
Q

For the Brainstem-spinal -indirect cortical control system (extrapyramidal), what does it control?

A

indirect control through the brainstem spinal pathway to spinal motor neurons

138
Q

In the pyramidal system (direct motor pathway) where do the axons arise from?

A

These axons arise from cells in all lobes of neocortex, but especially the frontal and parietal lobes

139
Q

In the pyramidal system (direct motor pathway) what is the path of the axons?

A

The cortico-bulbar tract descends through the brainstem and controls neurons of all the cranial nerve nuclei.

140
Q

Unilateral pathology of the cortico-bulbar tract (CB) will do what?

A

weaken movement of the head and neck on the opposite side of the body

141
Q

Why would unilateral pathology of the cortico-bulbar tract (CB) weaken movement of the head and neck on the opposite side of the body?

A

because most of the CB fibers arising, for example, on the left, will cross to control cranial nerve nuclei on the right side of the brain just rostral to the level of the cranial nerve nucleus being affected.

142
Q

For most of the cranial nerve nuclei there is also an ipsilateral component meaning what?

A

that they receive cortical input from the ipsilateral CB tract as well.

143
Q

Why would unilateral pathology of the CB tract not weaken significantly the muscles served by the cranial nerve nuclei on the opposite side below the level of injury or, in general, entirely remove cortical control of the cranial nerve nuclei?

A

Because there is also an ipsilateral component where that they receive cortical input from the ipsilateral CB tract as well. The bilateral projections from the surviving CB can sustain considerable movement on both sides of the patient

144
Q

For a unilateral CB lesion what are usually the only things affected?

A

usually only the tongue, (hypoglossal, CN 12) and face (facial, CN 7) are affected

145
Q

In the pyramidal system (direct motor pathway) what is the path of the cortico-pontine tract?

A

it descends to terminate on the pontine nuclei in the basis of the pons

146
Q

Axons from the pontine nuclei do in the pyramidal system (direct motor pathway)?

A

the nuclei forward the signals to the cerebellum on the opposite side

147
Q

Isolated damage to the cortico-pontine tract?

A

does not occur clinically

148
Q

In the pyramidal system (direct motor pathway) what is the path of the cortico-rubro-olivary circuit?

A

The cortex sends connections to a portion of the red nucleus that in turn projects to the inferior olive, the other major brainstem nucleus that projects to the cerebellum

149
Q

In the pyramidal system (direct motor pathway) what is the path of the cortico-spinal tract (CS)?

A

it descends through the brainstem and spinal cord.

150
Q

In the pyramidal system (direct motor pathway) what does the cortico-spinal tract control?

A

motor neurons of the trunk and limbs

151
Q

In the brainstem do CS axons descend on the same side or the opposite side as their cortical origin?

A

Same side

152
Q

Where does the CS axons cross?

A

most cross the midline in the caudal medulla (pyramidal decussation) continuing on the opposite side of the spinal cord (lateral corticospinal tract) to reach their targets.

153
Q

Do all of the CS axons cross?

A

No, only a small number of axons continue ipsilaterally (ventral/anterior corticospinal tract)

154
Q

In the pyramidal system (direct motor pathway) what does pathology in the brainstem result in?

A

it impairs movement mainly on the opposite side of the body.

155
Q

In the pyramidal system (direct motor pathway) what does pathology in the spinal cord result in?

A

if its below the decussation it will affect movement on the same side of the body.

156
Q

Usually what is seen in the pyramidal system (direct motor pathway) pathology?

A

Results in the damages the pyramidal and brainstem-spinal tracts together, causing marked weakness or outright paralysis of the affected muscles. The limbs become hyperreflexic over time

157
Q

In the few surgical case studies of isolated CS damage what was seen?

A

lesion of the medullary pyramid, the motor symptoms were modest: temporary weakness, permanent Babinski’s sign, and permanent loss of independent finger movements.

158
Q

In the brainstem-spinal pathways (indirect motor pathways), where do they originate?

A

In contrast to the pyramidal tracts, these pathways originate in the brainstem from nuclei

159
Q

What does the brainstem-spinal pathways (indirect motor pathways) collectively do?

A

they control the muscles of the neck, trunk and limbs.

160
Q

pathology in the brainstem will affect

A

movement on the opposite side of the body

161
Q

pathology in the spinal cord will affect

A

the movement of the same side of the body

162
Q

Isolated damage of the tracts in the brainstem-spinal pathways (indirect motor pathways) is?

A

rare clinically; in experimental studies damage becomes asymptomatic over time

163
Q

Motor Cortex controls what?

A

both the Pyramidal and Brainstem-spinal pathways

164
Q

Frontal lobe lesions often cause what?

A

severe paralysis

165
Q

Why do frontal lobe lesions often cause severe paralysis?

A

because the precentral (motor) and premotor areas of cortex contribute to both direct and indirect motor pathways

166
Q

What is the indirect motor pathway?

A

from the thalamic diagram that both the cerebellum and the globus pallidus project to VL and VA which in turn project to the motor and premotor cortices).

167
Q

Most of the axons of the pyramidal tract arise from where?

A

frontal gyri.

168
Q

Why does damage to the cortex affects the function of all motor pathways?

A

Since the frontal cortex sends axons to all the brainstem nuclei that project to the spinal cord (red nucleus, reticular formation, superior colliculus, vestibular nuclei, etc.) or affect motor control indirectly via the cerebellum (pontine nuclei, inferi

169
Q

What is the relationship between the cerebral cortex, basal ganglia and the premotor cortex?

A

the cerebral cortex also projects to the basal ganglia, which in turn controls both motor systems by virtue of projections from the globus pallidus that project to VA and VL and back to motor and premotor cortex.

170
Q

If the pathology is in the peripheral nerves where is it in relation to the symptoms?

A

it will lie on the same side as the symptoms.

171
Q

Why is it that the pathology of the peripheral nerves lies on the same side as the symptoms?

A

This is because peripheral nerves (e.g. dorsal roots, ventral roots, and all cranial nerves except the trochlear) do not cross.

172
Q

If the pathology is in the spinal cord where is it in relation to the symptoms?

A

spinal cord: it will be on the same side as all of the symptoms, except the pain and temperature loss.

173
Q

Why is it that the pathology of the spinal cord lies on the same side as the symptoms except the pain and temperature loss?

A

This is because the lemniscal and the motor tracts remain uncrossed through the spinal cord, but the AL tracts cross at or near the level of entry.

174
Q

If the pathology is in the brainstem where is it in relation to the symptoms?

A

it will lie on the same side as the most rostral symptom, but be on the side opposite the caudal symptoms

175
Q

Why is it that for the pathology of the brainstem the symptoms will lie on the same side as the most rostral symptom?

A

The most rostral symptom will tend to be caused by damage to the cranial nerve nucleus, or its axons that project ipsilaterally, so the s

176
Q

Why is it that for the pathology of the brainstem the symptoms will be on the side opposite the caudal symptoms?

A

. Caudal symptoms are due to damage to the descending motor axons that cross below the level of damage to innervate the cranial nerve nuclei, thereby causing symptoms on the opposite side (contralaterally).

177
Q

If the pathology is in the forebrain where is it in relation to the symptoms?

A

forebrain: it will lie opposite the symptoms

178
Q

Why is it that the pathology of the forebrain lies opposite to the symptoms?

A

This is because the pathways in the forebrain are not primary axons and are all crossed (except for the olfactory nerve).

179
Q

If the pathology is in the cerebellum is it in relation to the symptoms?

A

pathology will be on the same side as the symptoms.

180
Q

The peripheral motor neurons

A

actually contract the limb,

181
Q

The peripheral motor neurons are controlled by

A

several upper echelons necessary for normal movement, (e.g., motor cortex, pyramidal fibers, etc.).

182
Q

A normal muscle is

A

never entirely relaxed, but rather is kept in a state of moderate contraction.

183
Q

Normal muscle tone

A

state of moderate contraction and it can be felt in the resistance to passive movement of a person’s limb.

184
Q

What are the two factors by which tone is maintained?

A

1) the sensory fibers from muscle spindles 2) The Corticospinal and the indirect motor pathways

185
Q

Where do the sensory fibers from muscle spindles that help maintain tone synapse?

A

on motor neurons in the cord.

186
Q

How do the sensory fibers from muscle spindles maintain muscle tone?

A

They constantly excite the motor neurons with a baseline barrage of action potentials, which is partly responsible for the chronic partial contraction of the muscle.

187
Q

How do the Corticospinal and the indirect motor pathways help maintain muscle tone?

A

Descending motor tracts maintain a baseline level of excitability in the lower motor neurons.

188
Q

What keeps the muscle in their state of partial contraction?

A

The balance between excitability of motor neurons from the muscle spindles and descending motor tracts keeps the muscles in their state of partial contraction, which is called normal tone.

189
Q

How is muscle tone maintenance related to the deep tendon reflex?

A

This circuit is also responsible for the deep tendon reflex

190
Q

If you strike a normal muscle with a rubber hammer what happens?

A

it pulses the muscle spindles briefly, causing a sudden contraction of the muscle.

191
Q

What defines the normal deep tendon reflex?

A

The resulting jerk of the limb has a certain speed and amplitude

192
Q

When the resting contraction of the muscle is less than normal what is it called?

A

the tone is called “hypotonic” or “flaccid”, and the jerk of the limb when you hit it with your hammer is termed “hyporeflexic”.

193
Q

When the arm is stiffer and the reflex is snappier than normal what is it called?

A

the state is called hypertonic and hyperreflexic

194
Q

How might someone end up with a decrease in tone?

A

This could happen either by reducing sensory input to the cord from the spindles (e.g. dorsal root disease), or by reducing output from the cord to the muscles (e.g. ventral root disease).

195
Q

Any peripheral nerve disease, be it sensory or motor will produce what?

A

hypotonia and hyporeflexia

196
Q

The change in tone can sometimes serve as what?

A

An early warning sign since it is often detectable before the appearance of more obvious sensory loss or weakness

197
Q

How can you distinguish between dorsal (sensory) vs. ventral (motor) peripheral nerve damage?

A

1) if the lesion is severe enough; dorsal = loss of sensation, ventral = loss of movement 2) even if the lesion is slight; Loss of the motor neurons or nerves (e.g. Polio) triggers the death of the muscles innervated. Sensory nerve pathology does not caus

198
Q

How do muscles publicize their demise?

A

They do so very early with fasciculations (slight quiverings) and after a time atrophy will be apparent

199
Q

How would pathology of central descending motor tracts affect tone?

A

it will be lowered due to the sudden loss of descending connections

200
Q

How would pathology of central descending motor tracts affect the limb chronically?

A

Chronically the limb becomes hypertonic and hyperreflexic because the residual influence on motor neurons is predominantly excitatory

201
Q

Why is it that pathology of central descending motor tracts result in the limb becoming hypertonic and hyperreflexic?

A

There is no longer any descending input to counter the excitatory effect of the spindles.

202
Q

What does weakness accompanied by increased tone indicate?

A

that the pathology is not in the peripheral nerves, but somewhere along the course of the descending CNS motor tracts

203
Q

lower motor neuron paralysis

A

weakness accompanied by lowered tone and decreased reflexes is due to peripheral nerve damage (either sensory or motor nerves, or both)

204
Q

upper motor neuron paralysis

A

Weakness accompanied by increased tone and reflexes is due to damage to central motor pathways (descending tracts)

205
Q

When the facial nucleus or nerve is damaged what happens?

A

(lower motor neuron paralysis), the entire ipsilateral side of the face is weakened or paralyzed.

206
Q

If the pathology is in the left pons what is seen?

A

then the left half of the patient’s face is weak, from the forehead down to the chin. This points to pontine pathology where the facial nerve arises

207
Q

If the paralysis is of the “upper motor neuron” type, and is due to pathology of the forebrain, or the corticobulbar tract, then what is seen on the patient?

A

only the lower quadrant of the face will be paralyzed, and on the opposite side.

208
Q

If the left motor cortex is damaged what is seen on the patient?

A

the patient’s right lower quadrant of the face will be weak, but the right forehead, eyebrow, and orbicularis oculi muscles will be normal

209
Q

What is the explanation for the effect seen in paralysis of the upper motor neuron?

A

the corticobulbar axons from each side of the brain (motor cortex near the lateral sulcus) only have strong contralateral connections to facial motor neurons that innervate muscles of the lower half of the face.

210
Q

When the cerebral cortex is injured or the cortico-bulbar axons are damaged rostral to the facial nucleus, prior to where these axons decussate what is seen in the patient?

A

the muscles of the lower half of the face are paralyzed on the opposite side of the body.

211
Q

Why is it that when the cerebral cortex is injured or the cortico-bulbar axons are damaged rostral to the facial nucleus, prior to where these axons decussate the upper half of the face is not paralyzed?

A

because projections from the motor cortex and a region of the cortex concerned with emotional behavioral responses (a portion of the cingulate gyrus) both project bilaterally to motor neurons that innervate muscles in the upper half of the face.

212
Q

When the motor cortex or cingulate area is damaged, or the cortico-bulbar pathway on one side of the brain is damaged rostral to the facial nucleus what happens?

A

the remaining cortico-bulbar axons can compensate so little deficit is noted.

213
Q

Why is it that after middle cerebral artery damage, when contralateral lower facial paralysis is noted, patients can sometimes smile normally as an emotional response?

A

since the descending corticobulbar projection from the cingulate gyrus that projects bilaterally to facial muscles remains intact and can compensate so little deficit is noted

214
Q

What does loss of only a quadrant of facial movement point to?

A

damage of corticobulbar axons rostral to the pons, in the midbrain or forebrain, and on the opposite side of the body

215
Q

How does information leaves the two retinae?

A

by way of the two optic nerves

216
Q

At the optic chiasm

A

the two nerves partially decussate

217
Q

Axons from the nasal half of each retina

A

(temporal visual field) cross

218
Q

Axons from the temporal retina

A

(nasal visual field) do not.

219
Q

What happens to the retinal axons?

A

They enter the optic tract, which wraps around the thalamus and the crus cerebri

220
Q

What is the most important visual pathway?

A

Geniculo-calcarine pathway

221
Q

Damage to what pathway has the severest effect on vision?

A

Geniculo-calcarine pathway

222
Q

Where do most of the axons from the eyes terminate?

A

in the lateral geniculate nucleus (LGN) of the thalamus.

223
Q

What happens to the axons continue past the lateral geniculate nucleus?

A

They travel in the brachium of the superior colliculus to terminate in the pretectal area or nucleus on either side of the posterior commissure and others continue on to the superior colliculus

224
Q

What happens to neurons from LGN?

A

they project to the occipital lobe via the optic or visual radiations and terminate in primary visual cortex (V1, Brodmann area 17).

225
Q

What do the visual radiations wrap around?

A

they fan out and wrap around the lateral ventricles

226
Q

What is the path of the axons carrying information about the upper half of the visual field?

A

they pass deep to the cortex of the temporal lobe and terminate in the cortex of the inferior bank of the calcarine sulcus (lingual gyrus)

227
Q

What could eliminate some of your upper visual field?

A

pathology of the temporal lobe, or of the inferior bank of the visual cortex (lingual gyrus)

228
Q

What is the path for axons carrying information about the lower half of the visual field?

A

They pass deep to the parietal lobe and terminate in the cortex forming the superior bank of the calcarine sulcus (cuneus gyrus)

229
Q

What could eliminate some of your lower visual field?

A

damage to the parietal lobe or superior bank of visual cortex (cuneus gyrus) can result in scotomas in the lower visual field

230
Q

What does the hypothalamus pathway govern?

A

long-term reactions to light, e.g., resetting daily biological rhythms, detecting seasonal changes in light

231
Q

What projection from the hypothalamus is related to these seasonal changes in light?

A

One of the projections from the region of hypothalamus receiving optic input is to the pineal body,

232
Q

What is the location of the pretectal area or nucleus?

A

it lies at the transition between the thalamus and midbrain on either side of the posterior commissure.

233
Q

How are the pretectal nuclei connected?

A

There is a projection interconnecting the pretectal nuclei via the posterior commissure.

234
Q

How does the pretectal nucleus function?

A

like a light meter. It receives bilateral input from the two eyes and it contains cells that calculate the total light energy entering the eye.

235
Q

What happens to the cells that calculate the total light energy entering the eye?

A

These cells cross the midline to the other pretectal nucleus, or project to the Edinger-Westphal nucleus (EW) of the same side, the parasympathetic component of the oculomotor complex (III nucleus).

236
Q

What do the preganglionic EW axons project to?

A

They project with the third nerve to innervate the ciliary ganglion, which constricts the pupil in response to light.

237
Q

What is the function of the ciliary ganglion?

A

Constricts the pupil in response to light

238
Q

A loss of the reflex involved with the EW nucleus will lead to what?

A

a dilated pupil, and one that fails to constrict to a light being shined on the retina.

239
Q

The pupillary light reflex can be disrupted by pathology of

A

1) an optic nerve, 2) bilateral pretectal damage, or 3) pathology of CN 3.

240
Q

How can you determine whether the pathology is from the optic nerve, or bilateral pretectal damage, or to CN 3

A

By shining light in one eye of the patient and noting whether the same pupil constricts (direct pupillary reflex) and/or the opposite pupil constricts (consensual pupillary reflex) you can establish which of these three structures is involved.

241
Q

Direct pupillary reflex

A

shining light in one eye of the patient and the same pupil constricts

242
Q

Consensual pupillary reflex

A

shining light in one eye of the patient and the opposite pupil constricts

243
Q

What is the function of the Superior colliculus?

A

The function of this path in primates is uncertain, and no obvious visual symptoms attend pathology of the superior colliculus.

244
Q

The superior colliculus is certainly involved in what?

A

moving the eyes, head, and axial muscles. Some evidence suggests this optic input to the colliculus permits a very rapid orientation of our eyes and body to a visual event

245
Q

The vestibulo-cochlear nerve, CN8 does what?

A

it carries auditory information from the cochlea to the brain.

246
Q

Where does the vestibulo-cochlear nerve terminate?

A

in two nuclei, the dorsal and ventral cochlear nuclei,

247
Q

What is the location of the dorsal and ventral cochlear nuclei?

A

They lie on the surface of the inferior cerebellar peduncle at the transition of the medulla and pons.

248
Q

What does each CN8 carry?

A

information only from the one ear

249
Q

pathology of the left cochlea, or left CN8 or left cochlear nuclei will cause what?

A

deafness in the left ear

250
Q

For the auditory system, where do the second order neurons arise?

A

in the cochlear nuclei

251
Q

For the auditory system where do the second order neurons project to?

A

From the cochlear nuclei to several nuclei, and to both sides of the brain

252
Q

For the auditory system where do the projections of the second order neurons cross?

A

mainly in the caudal pons passing near the medial lemniscus in a region called the trapezoid body.

253
Q

Describe the flow of information along the brainstem for the auditory system.

A

about half of the information would ascend the brainstem on the left side, the other half on the right side. Thus, already at the second order of neurons, there is much bilateral mixing of information from the two ears. The mixing continues at every level

254
Q

A unilateral brainstem lesion at the second order axon and beyond (i.e. subsequent to the cochlear nuclei) will cause what?

A

It will not cause hearing deficits, because much of the information from both ears will escape injury

255
Q

What does it tell you if a patient has loss of hearing in one ear?

A

their pathology must be either in the ear, in CN8, or in the cochlear nuclei. It is not deeper into the brain than that.

256
Q

What do you know if the patient has hearing loss in both ears?

A

then the pathology must be bilateral. From the odds (and other symptoms) you must figure whether she has bilateral pathology in the ears, in the brainstem, or in the temporal lobe.

257
Q

Some axons of the cochlear nuclei terminate where?

A

in the superior olive and other nuclei (e.g. nucleus of the trapezoid body, nucleus of the lateral lemniscus). Other axons bypass these nuclei.

258
Q

All of the information for the auditory system eventually do what?

A

they ascend the brainstem in the lateral lemniscus.

259
Q

Much of the lateral lemniscus terminates where?

A

in the inferior colliculus.

260
Q

The inferior colliculus in turn projects to where?

A

the medial geniculate nucleus (MGN) of the thalamus

261
Q

How does the inferior colliculus project to the medial geniculate nucleus?

A

via a nerve tract seen on the surface of the midbrain between these two nuclei called the brachium of the inferior colliculus.

262
Q

MGN sends the information to where?

A

Heschl’s gyrus (transverse temporal gyri) in the cortex

263
Q

Heschl’s gyrus

A

(transverse temporal gyri) in the cortex

264
Q

How does the MGN send the information to where the Heschl’s gyrus?

A

by traveling through the posterior limb of the internal capsule, as do the other cortical projections from all the thalamic nuclei

265
Q

Heschl’s gyrus is called what?

A

primary auditory cortex (A1, Brodmann areas 41, 42) and is the primary sensory cortex for audition.

266
Q

What s the primary sensory cortex for audition?

A

Heschl’s gyrus

267
Q

What happens to the auditory information after Heschl’s gyrus?

A

it then projects to surrounding secondary auditory areas

268
Q

What is Heschl’s gyrus important for?

A

distinguishing sound patterns since information from both ears is processed bilaterally in the brain

269
Q

Damage to Heschl’s gyrus in only one hemisphere produces what? Explain.

A

A little deficit since information from both ears is processed bilaterally in the brain

270
Q

What mediates the perception of language?

A

Wernicke’s area which is the secondary auditory area located in the left hemisphere

271
Q

Damage to what structures result in an inability to understand spoken language?

A

1) Heschl’s gyri in both hemispheres or 2) damage to the left auditory cortex and the corpus callosum

272
Q

Why would you have to have damage to both left auditory cortex and the corpus callosum to produce an inability to understand spoken language?

A

Because the left Heschl’s gyrus receives projections from the right Heschl’s gyrus through the corpus callosum and since auditory information is cut off from Wernicke’s area in the left hemisphere (word deafness).

273
Q

Wernicke’s area includes

A

1) supramarginal gyrus 2) posterior portion of the superior temporal gyrus 3) planum temporale

274
Q

planum temporale

A

It also includes the flat area of cortex on the surface of the superior temporal gyrus within the lateral fissure posterior to Heschl’s gyrus

275
Q

Where are language functions largely centered?

A

in the dominant (left) hemisphere and involve more than one lobe.

276
Q

Where does the information about speech enter?

A

It enters the temporal cortex in Heschl’s gyrus and then spreads to Wernicke’s area.

277
Q

What happens to visual information related to reading?

A

Visual information from the occipital lobe that is related to reading enters Wernicke’s area via the angular gyrus.

278
Q

What happens to language information?

A

it is relayed to the frontal lobe, to Broca’s area in the inferior frontal gyrus, where the commands for speech are organized.

279
Q

“Wernicke’s aphasia”

A

(sensory or receptive aphasia) involves an inability to understand language and to speak coherently.

280
Q

In most cases Wernicke’s aphasia is associated with what?

A

damage to Wernicke’s area.

281
Q

“Broca’s aphasia”

A

(motor or expressive aphasia) is associated with an impaired ability to generate speech (including writing) and usually involves damage to Broca’s area.

Neuroscience - Unit 5 (12 decks)

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