Lab Quiz 4 Flashcards

1
Q

What cranial nerve arises from the lateral aspect of the mid-pons at the level of the middle cerebellar peduncles?

A

Trigeminal nerve

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2
Q

From where in the brainstem does the trigeminal nerve arise?

A

From the lateral aspect of the mid pons at the level of the middle cerebellar peduncles.

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3
Q

Lesions in corticospinal tract produce…

A

contralateral hemiparesis and Babinski’s sign

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4
Q

Lesions in the corticobulbar tract produce …

A

Contralateral lower facial palsy and dysarthria

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5
Q

Infarct of the pontine nuclei and pontocerebellar fibers causes…

A

contralateral ataxic hemiparesis (dysmetria + dysdidochockinesia)

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6
Q

What nerve arises from the dorsolateral aspect of the caudal pons at the pontomedullary junction, which is located at the level of the facial colliculus (below the middle cerebellar peduncles)?

A

The facial nerve

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7
Q

From where in the brainstem does the facial nerve arise?

A

From the dorsolateral aspect of the caudal pons at the pontomedullary junction, which is located at the level of the facial colliculus (below the middle cerebellar peduncles).

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8
Q

What CN arises from the preolivary sulcus at the level of the rostral medulla?

A

The hypoglossal nerve

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9
Q

From where in the brainstem does the hypoglossal nerve arise?

A

From the preolivary sulcus at the level of the rostral medulla.

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10
Q

What CN arises at the level of the superior colliculus and red nucleus (rostral midbrain)?

A

Oculomotor nerve

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11
Q

From where in the brainstem does the oculomotor nerve arise?

A

At the level of the superior colliculus and red nucleus, which are located in the rostral midbrain.

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12
Q

What CN arises from behind the midbrain at the level of the inferior colliculus (below the red nucleus?

A

The trochlear nerve

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13
Q

From where does the trochlear nerve arise?

A

From behind the midbrain at the level of the inferior colliculus (below the red nucleus).

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14
Q

Which cranial nerve decussates before innervating its target?

A

The trochlear nerve

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15
Q

Infarts involving the anterior portion of the medial pons can produce …

A

dysarthria and contralateral ataxic hemiparesis.

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16
Q

What happens with a lesion in the sensory cortex (parietal lobe)?

A

Contralateral hemianesthesia, astereognosis

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17
Q

What happens with a lesion in the superior parietal lobe?

A

Contralateral asterognosis and neglect

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18
Q

What happens with a lesion in the dominant inferior parietal?

A

Gerstmann[-ish] syndrome = dysgraphia, L/R confusion, finger agnosia, and dyscalculia +/= hearing loss

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19
Q

What happens with a lesion in the non-dominant inferior parietal?

A

Topographic memory loss, anosognosia, constructional and dressing apraxia, contralateral neglect, contralateral hemianopia/lower quadrantopia

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20
Q

What happens with a lesion in the bilateral posterior parietal?

A

Balint syndrome = optic ataxia + optic apraxia + simultagnosia

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21
Q

What is optic ataxia?

A

Inability to accurately reach for objects

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22
Q

What is optic apraxia?

A

inability to voluntarily guide eye movements/change to a new location of visual fixation

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23
Q

What is simultagnosia?

A

inability to perceive more than one object at a time, even when in the same place

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24
Q

Bilateral occipital lobe lesion

A

cortical blindness with intact pupillary response to light (Anton’s syndrome = denial of visual loss).

25
Q

Unilateral occipital lesion

A

contralateral hemianopia with or without macular sparing

26
Q

Occipital lobe and corpus collosum splenium lesion

A

“Alexia without agraphia”, patient can write but cannot read, even what they have just written.

27
Q

Primary auditory cortex

A

loss of hearing

28
Q

Wernicke’s area

A

fluent nonsensical speech, impaired comprehension

29
Q

Meyer’s loop

A

superior quadrantanopsia

30
Q

Olfactory bulb, tract, piriform cortex

A

ipsilateral anosmia

31
Q

Hippocampus

A

bilateral lesions give anterograde amnesia

32
Q

Anterior temporal lobe (amygdala)

A

Kluver-Bucy (visual agnosia, hyperphagia, hypersexuality)

33
Q

Inferomedial occipitotemporal cortex

A

bilateral lesions give prosopagnosia

34
Q

Disconnection between temporal and limbic cortices

A

Capgras syndrome

35
Q

basal region of L frontal lobe (L IFG)
superior division of L MCA
nonfluent, agrammatical, phonemic paraphasias comprehension intact
frustrated by deficit
neighborhood: dysarthria, right face/arm > leg weakness

A

Broca’s / Transcortical Motor / Anterior / Expressive:

36
Q

Broca’s / Transcortical Motor / Anterior / Expressive:

A

basal region of L frontal lobe (L IFG)
superior division of L MCA
nonfluent, agrammatical, phonemic paraphasias comprehension intact
frustrated by deficit
neighborhood: dysarthria, right face/arm > leg weakness

37
Q

Wernicke’s / Transcortical Sensory / Posterior / Receptive:

A

posterior L temporal-parietal junction (posterior third of STG, STS) inferior division of L MCA
fluent, nonsensical, semantic paraphasias
poor comprehension
often unaware of deficit (anosagnosia)
neighborhood: right (esp superior) visual field deficit (near Meyer’s loop of optic radiation)

38
Q

posterior L temporal-parietal junction (posterior third of STG, STS) inferior division of L MCA
fluent, nonsensical, semantic paraphasias
poor comprehension
often unaware of deficit (anosagnosia)
neighborhood: right (esp superior) visual field deficit (near Meyer’s loop of optic radiation)

A

Wernicke’s / Transcortical Sensory / Posterior / Receptive:

39
Q

Ability to repeat depends upon …

A

the arcuate fasciculus

40
Q

Expressive dysprosody

A

“Broca’s area” in non-dominant (right) hemisphere

cannot express emotion or inflection in speech

41
Q

Receptive dysprosody

A

“Wernicke’s area” in non-dominant (right) hemisphere - cannot comprehend emotionality or inflection in the speech

42
Q

Occlusion of which cerebral artery is of the greatest potential risk? Why? What larger vessel supplies this artery?

A

The middle cerebral artery supplies the mass of cortex on the lateral surface of the hemisphere as well as many subcortical structures. Occlusion of this artery unilaterally can lead to massive infarcts with dire consequences including unilateral paralysis, sensory loss and cognitive functions. It is also often fatal.

43
Q

What is a major origin of emboli to the MCA?

A

A major origin of emboli to the middle cerebral artery is from its parent vessel, the internal carotid artery.

44
Q

What is the most common site of emboli that eventually block the MCA?

A

The most common site of emboli formation is at the origin of the internal carotid artery, at the bifurcation of the common carotid arteries in the neck.

45
Q

Which major veins drain blood away from the cortex?

A

The superior and inferior sagittal sinuses drain blood away from the cerebral cortex to the internal jugular vein via the transverse sinus.

46
Q

What is the term used to designate cortical areas situated at the border between the territories supplied by two different cerebral arteries? What is the clinical significance of such zones?

A

Such border areas in the cerebral cortex are termed “border zones”, or more frequently but less accurately, “watershed areas”. These zones are particularly vulnerable to hypoxic/ischemic events. (The damage to the brain is most severe in the regions where the vascular supply is most tenuous, in the borderzones between vascular territories.)

47
Q

What are the major functions of primary sensory and motor areas? What deficit would result from damage to these areas?

A

The primary sensory and motor cortical areas provide the major channels of communication with the extrapersonal space. Lesions in each of the primary sensory areas causes nearly complete loss of function in the modality processed by that area. Damage to primary motor cortex leads to spastic paralysis.

48
Q

What are the major functions of unimodal association areas? What types of deficits would be caused by damage to these areas?

A

Each unimodal association area processes and integrates information related to a single modal- ity. Some unimodal association areas process information related to specific qualities of sensory information in regions sequentially removed from the primary areas. Such is the case with the visual association areas which process visual information related to color, motion, shape, objects, faces, words and targets. Damage to unimodal association areas causes selective perceptual deficits in the absence of general sensory loss.

49
Q

What are the major functions of multimodal association areas? What types of deficits would be caused by damage to these areas?

A

Multimodal association areas process information from two or more sensory and/or motor modalities. Damage to these areas always result in deficits which are multimodal and never confined to tasks which are under the guidance of a single modality. (e.g., cognitive or personality deficits)

50
Q

What are three major multimodal association cortical zones?

A

Prefrontal cortex.
Lateral temporo-parieto-occipital cortex
Medial temporo-parieto-occipital cortex

51
Q

The cerebral cortex projects to several other subcortical regions. Can you remember some of these projections?

A

The cerebral cortex projects to all three components of the brainstem, including the pons (cor- ticopontine) and medulla (corticobulbar) and to the spinal cord (corticospinal). In addition, widespread areas of cortex project to the striatum (caudate/putamen). The striatal output is directed towards the thalamus, which in turn projects back to the cortex, but this projection is not diffuse and is directed primarily towards motor and supplementary motor cortices.

52
Q

Broca’s area includes:

A

The foot of the precentral gyrus (also called the frontal operculum) and the area immediately anterior to it, often including the inferior frontal gyrus, or the white matter underneath it.

Lesions in this area cause Broca’s aphasia, or anterior aphasia. Patients have good comprehension. They can read. But they have great trouble generating speech (or written language) and produce short, non-grammatical, poorly articulated speech. The patient is usually frustrated. Although they can follow commands, they cannot repeat words or sentences spoken to them.

53
Q

Wernicke’s area includes:

A

the portion of the superior tem- poral gyrus located at the posterior banks of the lateral sulcus. These areas surround the transverse gyrus of Heschl, home of the primary auditory cortex.

Lesions in this region produce Wernicke’s aphasia, or poste- rior aphasia. This is a disorder of comprehension. It is much more variable than Broca’s aphasia, and there are many subtypes. Inability to read (for comprehension) or to follow commands, and the production of flu- ent speech with many errors are common.

54
Q

Lesion in what area causes conduction aphasia?

A

the supramarginal gyrus (in the inferior parietal lobule), extending inferiorly to the insula (area C).

Lesions in this area cause what is known as conduction aphasia. Simplisti- cally, such a lesion disconnects Broca’s and Wernicke’s areas (which are interconnected by a bundle of association fibers called the arcuate fasciculus), so the patient can comprehend, can speak adequately, but cannot transfer spoken speech effectively from temporal to frontal lobe, and hence cannot repeat words spo- ken to him.

55
Q

global aphasia

A

patient produces no use- ful speech, and displays poor comprehension

56
Q

What sites are activated when trying to pay attention?

A

The primary sites activated are part of the precentral gyrus in the frontal lobe (F), posterior parietal cortex (P) and anterior cingulate cortex (CG). As an oversimplification, attentional processing can be broken down into three distinct components: sensory (perceptual) = P, motor = F, and emotional = CG.

57
Q

A person with damage to the right posterior parietal cortex will have difficulty

A

perceiving sensory events in the left hemispace.

58
Q

Why doesn’t right hemisphere damage cause neglect on both sides, despite the fact that the right hemisphere is dominant for the processing of attention? What do you think would happen to attentional processing as a result of damage to the left hemisphere?

A

Left hemispheric damage can also produce contralateral neglect (on the right) but this syn- drome is less frequent, less severe and and not as lasting when compared with neglect caused by right hemi- sphere damage. Thus, neglect following right hemisphere damage is more noticeable and of greater clinical and behavioral significance because of its severity and enduring quality. Furthermore, careful clinical testing reveals that damage to the right hemisphere also produces a mild syndrome of neglect ipsilaterally, which is probably masked by the severity of neglect on the left. These facts, combined with fMRI studies, have led to the conclusion that the right hemisphere is capable of directed attention to both hemispaces (left and right) and that the left hemisphere exerts a weaker influence on attention to the right only. In such a scenario, a per- son with right hemisphere damage would show only very mild neglect on the right because of the weak com- pensation by the left hemisphere.

59
Q

Patients with pure prosopagnosia, in whom the only deficit is face recognition, display bilateral lesions in the …

A

fusiform gyrus (the gyrus located inferior to the calcarine sulcus, extending on the inferior surface of the brain into the temporal lobe).