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B&B Part 2 > B&B Week 7 > Flashcards

B&B Week 7 Flashcards

1
Q

what are primary areas of the cortex?

A

those that receive information from peripheral receptors via appropriate thalamic nuclei, with little interpretation of the meaning of that information

that include sensory and motor areas

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2
Q

where is the primary motor area?

A

the precentral gyrus of the frontal lobes (between the central sulcus and the precentral sulcus)

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3
Q

where does the precentral gyrus of the left hemisphere send motor output?

A

to the right side of the body (and vice versa)

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4
Q

the outflow from the primary motor cortex makes up what spinal tract?

A

the outflow from the primary motor cortex makes up the corticospinal tract

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5
Q

how are neurons in the primary motor cortex arranged?

A

neurons in the primary motor cortex are clustered in functional areas representing the various muscle groups they influence

this somatotropy carries forward as a somatotropic arrangement of fibres in the corticospinal tract and finally to the arrangement of LMNs in the anterior horn of the spinal cord

the size of body parts of the homonculus represents the size of the neuron pool supplying the musculature of that part of the body

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6
Q

what kinds of symptoms would arise if there was a lesion in the primary motor cortex?

A

a lesion in the primary motor cortex results in UPPER MOTOR NEURON signs similar to those that would be seen with a lesion anywhere along the cortisospinal tract

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7
Q

where is the supplementary motor area located?

A

anterior to the primary motor area and superior to the premotor area extending onto the medial surface of the hemisphere

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8
Q

the outflow from the supplementary motor area goes where?

A

neurons in this area send their efferents via the lateral corticospinal tract to innervate the truncal musculature for postural stabilization

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9
Q

where is the premotor association area located?

A

in the frontal lobe, just anterior to the primary motor area (inferior to the supplementary motor area)

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10
Q

what does the premotor association area do?

A

important for HIGHER ORDER processing and for INTEGRATING and INTERPRETING motor information and activity

plays a role in anticipating or “planning” a voluntary movement

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11
Q

where are the frontal eye fields located? what do they do?

A

in the premotor association area –> provide cortical control of gaze

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12
Q

what signs and symptoms would result from a lesion in the premotor association area?

A

APRAXIA –> a deficit in learned, skilled motor activity in the absence of paralysis (i.e brushing teeth, combing hair, whistling, blowing out a match)

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13
Q

where is the primary somatosensory area located?

A

composed of the postcentral gyrus of the PARIETAL lobe (on the opposite side of the central sulcus of the primary motor cortex)

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14
Q

where does the primary somatosensory cortex get its inputs from?

A

sensory afferents from the CONTRALATERAL peripheral receptors travel through the:
-PCML system
-spinothalamic tract
-trigeminal lemniscus/trigeminothalamic tract
to the sensory nuclei of the THALAMUS (VPL and VPM) then through the POSTERIOR limb of the INTERNAL CAPSULE and finally to the post-central gyrus

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15
Q

how are the neurons arranged in the primary somatosensory cortex?

A

somatotropic organization is preserved throughout the tracts resulting in a sensory homonculus

the size of the cortical representation is correlated with the tactile acuity in that part of the body

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16
Q

does the cortical representation of the body in the primary somatosensory cortex remain the same over time?

A

no, it is highly plastic

the area of the cortex that represents any particular body area can change over time in response to the input or lack thereof from a particular area of the body

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17
Q

where does the phenomenon of lateral inhibition of sensation occur?

A

the concept of lateral inhibition to increase tactile acuity occurs both in peripheral tissues and at the cortical level–> an area that receives sensory input send inhibitory projections to adjacent areas, thereby increasing the contrast between an area receiving input and one not receiving input

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18
Q

what kind of signs and symptoms would you expect in someone who had a lesion in the primary somatosensory cortex?

A

a lesion in the primary somatosensory cortex typically does NOT result in a complete loss of sensory perception–> results rather in a deficit in the awareness of sensory input and poor localization of sensory stimuli

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19
Q

where is the somatosensory association area located?

A

located adjacent to the primary sensory area in the parietal lobe (posterior)

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20
Q

what is the function of the somatosensory association cortex?

A

critical for allowing for the interpretation of the significance of sensory information

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21
Q

what signs and symptoms can you expect in a person with a lesion in the somatosensory association cortex?

A

either TACTILE AGNOSIA (a deficit in the ability to combine touch, pressure and proprioceptive input to interpret the significance of sensory information)

or

ASTREOGNOSIS (inability to recognize an object placed in the hand)

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22
Q

where is the primary visual cortex located?

A

consists of the area of of the cortex on either side of the CALCARINE SULCUS on the medial side of the occipital lobe

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23
Q

describe the pathway of afferents that enter the primary visual cortex

A

afferent fibres from the RETINA project to the LATERAL GENICULATE NUCLEUS which then sends fibres known as OPTIC RADIATIONS to the primary visual cortex

the right side of the visual cortex received information from the right retina/left visual field and vice versa

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24
Q

how are the neurons in the primary visual cortex arranged?

A

retinopically organized

the region of the fovea is represented near the occipital pole, while more peripheral regions of the ipsilateral retinas and contralateral visual fields are represented more anteriorly long the calcarine fissure

because it is the region of highest density of photoreceptors and correspondingly high visual acuity, the fovea has a disproportionate cortical representation, occupying about 50% of the primary visual cortex

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25
Q

what amount of the primary visual cortex is dedicated to the fovea?

A

50%

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26
Q

what signs and symptoms would you expect in someone with a lesion in the primary visual cortex?

A

deficit in vision in the OPPOSITE visual field

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27
Q

where is the visual association area found?

A

the area of cortex surrounding the primary visual cortex on the medial surface and extending onto the lateral surface of the occipital lobes

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28
Q

what is the function of the visual association area?

A

serves to give meaning and interpretation to what you see

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29
Q

what signs and symptoms would you expect in a person with a lesion in the visual association area?

A

VISUAL AGNOSIA–> deficit in the ability to recognize objects in the OPPOSITE visual field despite intact vision

it can also result in a deficit in pursuit or tracking of an object IPSILATERALLY

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30
Q

where is the primary auditory area located?

A

deep within the lateral sulcus, on the superior surface of the superior temporal gyrus of the temporal lobe

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31
Q

describe the pathway of the inputs to the primary auditory area

A

information from the COCHLEA projects to the MEDIAL GENICULATE nucleus of the thalamus, which in turn projects to the primary auditory cortex

ascending info from the cochlea travels both ipsilaterally and contralaterally such that each ear is represented BILATERALLY on the auditory cortex

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32
Q

what signs and symptoms would you expect in a person with a lesion in the primary auditory area?

A

decreased perception of sound, primarily in the CONTRALATERAL ear (info from contralateral cochlea predominates)

complete loss of hearing limited to one side would occur with a lesion of the hair cells or auditory nerve on that side

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33
Q

where is the auditory association area found?

A

adjacent to the primary auditory area on the lateral surface of the superior temporal gyrus

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34
Q

what is the function of the auditory association area?

A

allows us to interpret the sounds we hear and give them meaning

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35
Q

what signs and symptoms would you expect in a person with a lesion in the auditory association area?

A

ACOUSTIC VERBAL AGNOSIA (word deafness) –> ability to interpret what is heard is compromised despite intact hearing

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36
Q

where is the cortical representation of taste found?

A

located in the INSULA, which lies deep within the lateral sulcus

info reaches the insula from the taste receptors through the VPM of the thalamus

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37
Q

where is cortical representation of the olfactory sense found?

A

on the inferior and medial surface of the brain, in the ENTORHINAL cortex as well as the inferior portions of the TEMPORAL lobe (primary olfactory cortex)

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38
Q

what are association areas?

A

receive input from the primary area it is associated with, and, usually, from the appropriate thalamic relay nuclei as well

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39
Q

what is the function of association areas in general?

A

involved in higher order processing and integrating and interpreting information

characteristics that we would describe as being profoundly human, such as those that determine our personality, guide our decision making and store our memories and knowledge, are all processed in association areas

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40
Q

where are the frontal association areas?

A

occupy the frontal lobes anterior to the motor and sensory areas and are referred to as the PREFRONTAL CORTEX

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41
Q

what are the two regions of the prefrontal cortex, and what are they each responsible for?

A
  1. dorsal and lateral parts–> connected with sensory and motor cortex, basal ganglia and cerebellum; serve to regulate ATTENTION and MOTOR responses to STIMULI
  2. ventral and medial parts–> connected with the amygdala, hypothalamus and nucleus accumbens; serves to regulate EMOTIONS
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42
Q

list the functions of the frontal association areas/prefrontal cortex

A
  1. directing and maintaining attention (executive function)
  2. problem solving (executive function)
  3. morality
  4. adjusting behaviors to social norms
  5. working memory
  6. deliberate decisions
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43
Q

what happens if someone damages their frontal lobe?

A

damage to the frontal lobe leads to changes in personality and loss of the ability to demonstrate appropriate behaviors, without, necessarily, the loss of intellectual capacity (i.e the cage of phineas gage)

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44
Q

what structures does the prefrontal cortex communicate with in order to regulate attention and motor response to stimuli?

A

basal ganglia and cerebellum

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45
Q

where are the parietal association areas located?

A

posterior to the primary sensory areas in the post central gyrus

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46
Q

what is the function of the parietal association areas?

A

critical in ATTENTION and in the AWARENESS OF SELF and EXTRAPERSONAL SPACE

processes the position and movements of objects, people or self in space

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47
Q

what does the right posterior parietal cortex do? how about the left?

A

right–> orients our attention in SPACE

left–> orients our attention in TIME

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48
Q

why do the posterior parietal cortices and the prefrontal cortex communicate?

A

communications between these areas allow the prefrontal cortex to decide which stimulus to focus on by filtering out distractions

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49
Q

what happens if you get a lesion in the posterior parietal cortex in the NON-dominant hemisphere?

A

(typically the right is the non dominant hemisphere)

a lesion here can lead to CONTRALATERAL NEGLECT SYNDROME

stimuli in the environment on the side opposite the lesions are ignored

the neglect includes both lack of awareness of extrapersonal space and lack of awareness of self on the side opposite the lesion

i. e
1. patient fails to dress left side of body/shave left side of face
2. patient fails to draw the left side of a figure

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50
Q

how does processing of the right side of extrapersonal space differ from that on the left?

A

interestingly, attention to the right side of extrapersonal space and of self is mediated by BOTH the right and left posterior parietal lobes so that a lesion on one side would be compensated for by input from the other

thus, a lesion to the dominant hemisphere (i.e the left) typically results in TACTILE AGNOSIA (damage to parietal lobe and thus somatosensory deficits) rather than contralateral neglect syndrome

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51
Q

what happens if you get a lesion in the posterior parietal cortex in the dominant hemisphere?

A

interestingly, attention to the right side of extrapersonal space and of self is mediated by BOTH the right and left posterior parietal lobes so that a lesion on one side would be compensated for by input from the other

thus, a lesion to the dominant hemisphere (i.e the left) typically results in TACTILE AGNOSIA (damage to parietal lobe and thus somatosensory deficits) rather than contralateral neglect syndrome

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52
Q

what are the temporal association areas?

A

represent regions of the temporal lobe that are connected with the task or recognizing stimulus patterns

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53
Q

where is the visual stimulus of a face or an object linked to the recognition of its meaning or identity?

A

medial surface of temporal lobe, specifically the FUSIFORM GYRUS

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54
Q

what is the function of the lateral surface of the temporal lobe?

A

recognition of patterns related to LANGUAGE

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55
Q

what does it mean when you say that the temporal association areas appear to be lateralized?

A

the ability to recognize faces appears to be located predominantly on the RIGHT side of the interior temporal cortex

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56
Q

what happens if you get damage to the temporal lobe association areas?

A

can lead to AGNOSIA (inability to recognize or identify objects or people)

PROSOPAGNOSIA refers to the inability to recognize the faces of people you are familiar with

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57
Q

what defines the dominant hemisphere?

A

location of the language areas (which are highly lateralized)

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58
Q

in what % of RIGHT handed people would you find the main centers of language in the LEFT hemisphere?

A

98%

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59
Q

in what % of LEFT handed people would you find the main centres of language in the LEFT hemisphere?

A

70%

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60
Q

what role does the non-dominant (usually right) hemisphere play in language?

A

contributes to language through the melody (prosody), rhythm, emotional expression and accent

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61
Q

what are the two major language centers found in the dominant hemisphere?

A

broca’s and wernicke’s areas

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62
Q

what connects broca’s and wernicke’s areas?

A

a subcortical bundle of white matter–> ARCUATE FASCICULUS

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63
Q

where is broca’s area located?

A

in the inferior frontal gyrus of the FRONTAL LOBE

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64
Q

what is broca’s area responsible for?

A

PRODUCTION of language, including written, spoken and sign language

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65
Q

what is wernicke’s area responsible for?

A

COMPREHENSION of language, both signed and spoken–> allows us to interpret and assign meaning to symbols

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66
Q

where is wernicke’s area located?

A

superior TEMPORAL gyrus and extends around the posterior end of the lateral sulcus into the parietal region

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67
Q

what does the arcuate fasciculus do?

A

connects wernicke’s and broca’s areas

serves to monitor speech and facilitates the repetition of words

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68
Q

what happens if get a lesion to the primary language areas?

A

leads to APHASIA–> inability to communicate effectively

the type of aphasia depends on which area is damaged

**aphasias are distinct from dysarthrias (in which the production of language is impaired due to a lesion to the muscles of the larynx, pharynx, tongue or the nerves that supply those structures)

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69
Q

what is affected in Broca’s aphasia? what type of speech would you expect?

A

this is an expressive or productive aphasia–> non fluent, telegraphic speech

difficulty with syntax, grammar, and production of individual words

comprehension is intact

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70
Q

what is affected in Wernicke’s aphasia? what type of speech would you expect?

A

this is a receptive or sensory aphasia–> produces nonsensical ramblings, neologism

fluent speech, syntax and grammar, and the structure of words is intact

difficulty with comprehension of speech

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71
Q

what is a conduction aphasia?

A

difficulty repeating words –> both comprehension and production of language are intact

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72
Q

what is the role of the thalamus?

A

gatekeeper of the cortex

it is the target of all sensory information (except olfaction) on the way to the cortex

subcortical structures project to the cortex via the thalamus to influence UMN motor output

the thalamus also connects cortical structures with each other–> integrates, modulates and gates the flow of information from one part of the cortex to the other

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73
Q

what are intra-hemispheric (association) fibres?

A
  1. short association fibres–> connect cortical areas in adjacent gyri
  2. long association fibres–> connect cortical areas that are further removed, but still intrahemispheric
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74
Q

where is the superior longitudinal fasciculus, and what does it do?

A

most compact, above the insula

connects frontal, parietal and temporal cortical areas

connects wernicke’s area in the posterior end of the lateral sulcus with broca’s area in the inferior frontal gyrus (arcuate fasciculus is part of the SLF)

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75
Q

where is the inferior occipitofrontal fasciculus, and what does it do?

A

below the insula

connects frontal, temporal, and occipital lobes

fibres emerge to hook around the lateral fissure to connect the frontal and temporal cortex–> uncinate fasciculus

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76
Q

where is the superior occipitofrontal fasciculus?

A

adjacent and perpendicular to the corpus callosum

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77
Q

where is the cingulum?

A

runs beneath the cingulate and parahippocampal gyrus and connects the limbic cortex

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78
Q

what are commissural fibres?

A

reciprocal connections between corresponding areas of both hemispheres

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79
Q

where do the majority of the commissural fibres cross?

A

via the corpus callosum

body connects the frontal and parietal lobes

splenium (posterior) connects occipital lobes and posterior temporal lobes

genu (anterior) connects the frontal areas

fibres fan out to all parts of the cortex as the corpus callosum approaches the medulla –> forceps minor anteriorly and forceps major posteriorly

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80
Q

what does the anterior commissure connect?

A

connects two anterior temporal lobes and olfactory bulbs

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81
Q

what does the posterior commissure connect?

A

connects to the pretectal nuclei (between the thalamus and the midbrain)

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82
Q

what are projection fibres? what do they do?

A

connect to and from cortex (two way traffic between thalamus and cortex)

descending fibres (to striatum, brainstem and spinal cord) are a fan beneath the cortex–> corona radiata–> internal capsule (compact)

**optic radiations are fibres running from the LGN of the thalamus to the visual cortex

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83
Q

what fibres are found in the anterior limb of the internal capsule?

A

corticopontine fibres

thalamocortical fibres *from dorsomedial and anterior nuclei

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84
Q

what fibres are found in the genu of the internal capsule?

A

corticobulbar fibres

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85
Q

what fibres are found in the posterior limb of the internal capsule?

A

corticopontine fibres

thalamocortical fibres *from VP, VL and VA

corticospinal fibres

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86
Q

what is the blood supply to the anterior limb of the internal capsule?

A

lenticulostriate arteries (deep branches from middle and anterior cerebral arteries)

anterior cerebral artery

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87
Q

what is the blood supply to the genu of the internal capsule?

A

anterior choroidal arteries

88
Q

what is the blood supply to the posterior limb of the internal capsule?

A

anterior choroidal arteries

lenticulostriate arteries (deep branches from MCA)

89
Q

what structures supply blood to the cortex?

A

circle of willis

90
Q

what arteries supply blood to the forebrain?

A

anterior, middle and posterior cerebral arteries (ACA, MCA, PCA)

–> these arteries are all “end arteries” meaning they do not have connections with other arteries, with little to no overlap in their territories

91
Q

what is a “watershed area”? what is important about them clinically?

A

an area where two arteries’ perfusion territories come together

watershed areas are the most vulnerable when BP drops or hemorrhage in a central vessel occurs

92
Q

where does the ACA branch off of? where does it go? what does it supply?

A

branches off the circle of willis and travels into the INTERHEMISPHERIC FISSURE along the superior surface of the corpus callosum

it supplies the medial surface of the frontal and parietal lobes and 1-2 cm of the lateral surface of the frontal and parietal lobes

deep branches supply the head of the caudate nucleus and the anterior limb of the internal capsule

93
Q

where does the MCA branch off of? where does it go? what does it supply?

A

direct branch off the internal carotid

largest artery supplying the cerebral hemispheres

travels through the lateral fissure onto the lateral hemisphere

supplies almost the entire lateral surface of the cortex

94
Q

what do the lenticulostriate arteries supply?

A

basal ganglia and portions of the internal capsule

they are small vessels and are vulnerable to rises in BP–> weaker arterial walls may not be able to withstand high pressure–> this can lead to hemorrhagic stroke in the internal capsule and basal ganglia

95
Q

where does the anterior choroidal artery branch off of? where does it go?

A

from the internal carotid artery –> goes to the choroid plexus in the lateral ventricle

96
Q

what structures are supplied by the anterior choroid artery?

A

hippocampus

inferior part of the posterior limb of the internal capsule

tail of the caudate nucleus

97
Q

where does the posterior cerebral artery branch off of?

A

branches off the basilar artery at the rostral end

connected to the internal carotid system through the posterior communicating arteries

98
Q

what does the PCA supply?

A

medial surface of the occipital lobe and the interior and medial parts of the temporal lobe, the splenium of the corpus callosum

deep branches supply the thalamus and parts of the midbrain

99
Q

what are the 3 major types of cerebrovascular disease?

A

ischemic stroke

hemorrhagic stroke

vascular malformation

100
Q

list the types of intracerebral hemorrhage

A
  1. epidural–> between dura and skull
  2. subdural–> between dura and parenchyma (bridging veins)
  3. subarachnoid–> main blood vessels between arachnoid and pia
  4. intraparenchymal–> into brain
  5. intraventricular
101
Q

what is a common cause of intraparenchymal hemorrhage?

A

hypertension

deep structures are more susceptible to stroke because they are fed by small perforating arteries that can have small aneurysms

even small amounts of bleeding can devastate deep brain structures

102
Q

what is amyloid angiopathy?

A

can cause intraparenchyma hemorrhage

amyloid protein is deposited into vessel walls–> makes the walls fragile and weak

characteristic microscopic histology–> green rings showing amyloid deposits

103
Q

what are aneurysms? what type of cerebrovascular event do they usually cause?

A

either saccular (berry) or fusiform (sausage) in shape

arterial weakening usually at branch points–> occur at bifurcations and “bubble” expands in direction of flow

common cause of subarachnoid hemorrhage

cerebral arteries are susceptible–> thin media (muscle) and intima, with “medial defects” media has gaps where the muscle is absent and aneurysms form; they are relatively small arteries; lack external elastica

104
Q

when should you treat an unruptured aneurysm?

A

if its more than 5 mm

105
Q

what are some causes of subarachnoid hemorrhage?

A

cerebral aneurysms–> most common cause

vascular malformation

trauma

106
Q

what is the most worrisome result of a subarachnoid hemorrhage?

A

increased ICP

it is a life threatening condition and management is critical

107
Q

how do subarachnoid hemorrhages present?

A

“worst headache of my life”–> thunderclap headache

nausea, photophobia

sudden death

ANY patient presenting with sudden, severe headache should be considered as having a subarachnoid hemorrhage until proven otherwise

108
Q

what are the pathological features of subarachnoid hemorrhage?

A

increased ICP and cerebral edema

cranial nerve injury

hydrocephalus due to CSF flow interruption

109
Q

how do you diagnose and classify subarachnoid hemorrhage?

A

grade 1 (mild and asymptomatic)–> grade 5 (coma)

lumbar puncture and cerebral angiography

110
Q

what are some complications associated with subarachnoid hemorrhage?

A

recurrent bleeding

111
Q

what are clinical features of a cerebral vascular malformation?

A
  1. hemorrhage/bleeding in the subarachnoid space
  2. focal neurology, location development
  3. headache
  4. seizures from ischemia–> glial scar around the malformation from oxygen starvation
112
Q

how do you grade cerebral vascular malformations?

A

size

location (eloquence–> area with specific function i.e hearing or vision)

deep venous drainage–> superior/cortical surface of deep brain

113
Q

how do you treat cerebral vascular malformations?

A
  1. embolization (crazy glu into the malformation to block it off)
  2. no intervention
  3. microsurgery
  4. combination tx
114
Q

what is an ischemia stroke?

A

inadequate cerebral perfusion and cell death in the brain –> large or small vessel

location can be supratentorial or into brainstem

115
Q

what are the two cerebral ischemic syndromes?

A

transient ischemic attack (TIA)

infarction/stroke

116
Q

how do you diagnose an ischemic stroke?

A

CT scan within the first few hours may be “clean” after a stroke–> this is good because it means it may be early enough to intervene

MRI can show stroke lesion immediately, especially DWI weighted

117
Q

what are the goals of ischemic stroke tx?

A

prevent or reverse brain injury

118
Q

list possible treatments for ischemic stroke

A
  1. thrombolysis (TPA)
  2. anticoagulants
  3. anti-platelet antigens
  4. medical support
119
Q

what is the standard thrombolysis (TPA) treatment for ischemic stroke?

A

standard treatment bolus + IV within 3 hours

bigger clots, you can do intra-arterial TPA via femoral catheter –> with this tx you have a 6 hour time window, you get direct delivery of the thrombolytic agent, can use a lower dose, have lower systemic effects and you increase the rate of clot lysis

120
Q

what is the most common cause of thromboembolic stroke?

A

carotid stenosis

atherosclerosis of the arteries–> ie due to smoking, HTN, hyperlipidemia, diabetes, obesity

121
Q

what are the symptoms of carotid ischemia?

A

unilateral weakness and numbness, dysphagia if occurs in dominant hemisphere

122
Q

how do you evaluate a suspected carotid ischemia?

A

CT angiogram is the gold standard

arterial carotid bruits/neuro exam

123
Q

how do you treat carotid ischemia medically?

A
  1. antiplatelets
  2. BP control
  3. lipid profile
  4. smoking cessation
124
Q

how do you treat carotid ischemia surgically?

A

revascularization

stenting (endarterectomy)

being symptomatic is a strong indication for revascularization; asymptomatic carotid ischemia is a modest indication

125
Q

what is the third most common cause of death in western society?

A

stroke

after heart disease and cancer

126
Q

what is the most common cause of disability in western society?

A

stroke

127
Q

what is the most costly, common and important neurologic disease in adults?

A

stroke

128
Q

what is the penumbra?

A

in stroke, it is the dysfunctional but salvageable tissue

129
Q

if you have symptomatic carotid stenosis, what is the % risk you will have a disabling stroke within one year?

A

25%

130
Q

list 3 symptoms of carotid ischemic symptoms

A
  1. unilateral weakness/numbness
  2. dysphagia
  3. amaurosis fugax
131
Q

what is amaurosis fugax?

A

symptom of carotid ischemia

a painless transient monocular or binocular visual loss (i.e., loss of vision in one or both eyes that is not permanent).

132
Q

why is tissue imaging important in cerebral ischemia/stroke?

A

discriminate between infarction and ischemic penumbra

133
Q

what is TPA?

A

tissue plasminogen activator

134
Q

how effective is TPA in the treatment of ischemic stroke?

A

patients treated with IV tPA within 3 hours of the onset of symptoms were at least 30% more likely to have minimal or no disability at 3 months –> benefit was not associated with an increase in mortality

there is a risk of hemorrhage though

135
Q

where are the 3 most common locations in terms or cerebral arteries for an aneurysm?

A
  1. anterior communicating artery (30%)
  2. posterior communicating artery (25%)
  3. middle cerebral artery (20%
136
Q

what is the most common cause of primary subarachnoid hemorrhage?

A

ruptured aneurysm

137
Q

what are 4 “states” of cognition? what about 4 “channels” or cognition?

A 
state:
arousal
attention
mood
motivation
channek:
language
memory
visuospatial function
somatomotor function
138
Q

what must you have in order to have attention?

A

arousal and alertness

139
Q

what is the “bedrock” of cognition?

A

attention

has both state and channel components

140
Q

how would you characterize inattention?

A

it may be:
1. generalized (i.e confusional state/delirium)

  1. restricted to one side of space (i.e hemispatial neglect)
  2. modality-specific (i.e auditory vs. visual)
141
Q

what structures mediate attention?

A

brainstem

basal ganglia

thalamic and cortical structures

142
Q

define attention

A

the ability to engage and maintain salient stimuli in consciousness while extruding irrelevant perceptions, thoughts and feelings

143
Q

what are the neuroanatomical correlates of attention?

A
  1. cortical–> reticular formation of ascending sensory info
  2. frontal contribution–> focusing requires conscious voluntary effort (i.e studying)
  3. paralimbic input–> adds emotional importance to attention (i.e fear of failure)
  4. paralimbic influences may be critical for selective attention (i.e screening out extraneous stimuli)
  5. brainstem and basal forebrain cholinergic projections play an important circuit-tuning role (this can be related to anticholinergic delerium)
  6. parietal cortices are involved in shifting from one spatial locus of attention to another
  7. activation of a distributed cortical network may be required for conscious awareness
144
Q

what advantage does the MoCA have over the MSSE?

A

has more tools to test memory specifically

145
Q

list some bedside tests of working memory/attention

A
  1. digit span–> tests span of apprehension; can normally repeat 5-7 digits forwards
  2. to test “mental control” or working memory:
    - reverse digit span should be approx. the length of time of forward digit span minus 2 (i.e if 6-7 forwards, should be at least 5 backwards)
    - months backwards may be better screen in elderly
    - days of the week backwards if unable to do months
    - spelling “world” backwards (same as MSSE)
146
Q

in what % of hospitalized patients do you get delirium?

A

10-30%

may be presenting feature of an undiagnosed medical illness

can be life threatening in and of itself (i.e delirium tremens) and you can have increased risk of complications i.e hip fracture, DVT, aspiration)

147
Q

what mortality rate within 6months of discharge is associated with delirium while hospitalized?

A

25% mortality rate within 6 months of discharge

148
Q

what is a frequent cause of delirium in hospitalized patients?

A

iatrogenic

149
Q

what are the cardinal features of delirium?

A

severe attentional disturbance

distractability–> impaired vigilance and “concentration”

disorientation in an indication of severity (may fluctuate, may not always present in mild cases)

fluctuating arousal/somnolence–> “sundowning” and disturbance in sleep/wake cycles

fragmentation of thought and action

perseveration, motor impersistence (frontal contribution)

moment-to-moment fluctuations in performance on cognitive tests

150
Q

define delirium

A

a confusional state + illusions, hallucinations (especially visual and tactile)

a clinical syndrome characterized by prominent, fluctuating disturbance of attention and sometimes arousal and hallucinations, with a protean differential diagnosis

151
Q

what are the mechanisms behind delirium?

A

disrupted modulation of neocortical function and thalamocortical transmission by bioaminergic projections

  1. interruption or destruction of bioaminergic projection systems (i.e infarction, diffuse axonal injury)
  2. receptor mediated effects (i.e blockade, up or down regulation, altered modulation of receptors)
  3. interference with NT release
  4. impaired synthesis of NTs
  5. electrochemical (i.e hyponatremia, hypercalcemia)
  6. other metabolic derangements
152
Q

what role do derangements of cholinergic neurotransmission play in delirium?

A
  1. interference with cholinergic transmission–> i.e ACh receptor blockade (many drugs) or reduced ACh release (dopamine agonists, opioids, barbituates, alcohol)
  2. impairment of bioamine synthesis by ChAT (hypoxia, hypoglycemia, thiamine deficiency)
  3. deficiency of methyl donors (serine and methionine) which are important for ACh production
153
Q

what is a mnemonic to remember the DDx for delirium?

A

STAT VITAL SIGNS

Stroke
Toxic/metabolic encephalopathy
Autoimmune/inflammatory disorders
Thyroid disorders

Vitamin deficiencies (ie. thiamine, niacin, B6)
Infection
Trauma
Alzheimer’s disease
Liver, kidney, cardiac (major organ) failure

Surgery 
Iatrogenic
Geriatric 
Neoplasia 
Seizures
154
Q

what are the most common causes of delrium?

A
  1. fever–>especially in children
  2. infection–> most commonly pneumonia, bladder infections or sepsis, but meningitis and encephalitis need to be ruled out
  3. chemical disturbances and energy failures–> hyponatremia, uremia, hypoglycemia, hypoxemia, hypercarbia, hyperammonenia due to liver failure, thyroid dysfunction, THIAMINE deficiency
  4. withdrawal/intoxication–> alcohol, benzos, barbituates, other sedatives that increase GABAergic tone
  5. drugs–> especially primary and secondary anticholinergic drugs, opioids, lithium and anticonvulsant toxicity, antiparkinsonian agents, drugs of abuse
    * can be caused by focal/multifocal lesions, especially right hemisphere strokes
    * can be caused by autoimmune processes (CNS lupus, paraneoplastic syndromes)
155
Q

list some right hemisphere syndromes

A
  1. constructional apraxia
  2. spatial and topographical disorientation
  3. dressing impairment/”dressing apraxia”
  4. hemi-neglect and anosagnosia
  5. emotional indifference
  6. language alterations, aprosodias
  7. alterations in “pragmatics” of speech
156
Q

what is anosognosia?

A

unawareness of deficit (i.e in hemi-spatial neglect)

157
Q

when patients get hemi-spatial neglect, which side is usually affected?

A

its usually left sided neglect, due to lesions in the right (non-dominant) hemisphere

158
Q

what are the four types of memory?

A
  1. episodic –> last time you rode a bike; “recall of recent events”
  2. semantic–> knowing what a bike it
  3. procedural–> knowing how to ride a bike
  4. working–> taking bike lock key and house key on the way to ride your bike
159
Q

what structures are associated with semantic memory?

A

inferolateral temporal lobes

160
Q

what structures are associated with procedural memory?

A

basal ganglia (putamen)

cerebellum

supplementary motor area

161
Q

what structures are associated with working memory?

A

prefrontal cortex

162
Q

what is episodic memory?

A

the memory system for temporally specific events (i.e beginning and ending in time)

episodes which are “personally experienced”

autobiographical form of memory for contextually specific events

163
Q

what are some bedside tests to test for episodic memory?

A
  1. recent event recall (medical hx, family events, meals, major news items)
  2. word lists (MoCA 5 word list)
  3. paragraph recall
  4. three word, three shape test
  5. three bedside objects and locations
164
Q

what structures are associated with episodic memory?

A

episodic mesial temporal lobes–> hippocampus, parahippocampal gyrus

+

fimbria/fornix, mammillary bodies, mamillothalamic tract, anterior thalamic nuclei and the cingulate gyrus

165
Q

what is the most common cause of procedural memory loss?

A

parkinson’s

166
Q

what are the cognitive functions associated with the frontal lobe?

A
  1. divided and selective attention
  2. retrieval from semantic and episodic memory
  3. abstraction, analogical reasoning
  4. “switching gears”
  5. insight
  6. judgement, assessment of reward
  7. planning and problem solving
167
Q

what role do the frontal lobes play in behavior?

A
  1. motor activation (apathy)
  2. aspects of personality
  3. social judgement and demeanor
  4. empathy and consideration of the rights and feelings of others
  5. interest in personal hygiene and grooming
168
Q

what is orbitofrontal syndrome?

A

i.e cracking jokes that no one else finds funny

  1. disinhibition
  2. impulsive behavior
  3. distractable
  4. emotional lability, irritable
  5. inane euphoria
  6. jocularity
  7. poor judgement and insight
  8. hyperactive/manic-like presentation
  9. sexual disinhibition
169
Q

how does a semantic aphasia manifest?

A

social faux pas

170
Q

what is dorsolateral frontal syndrome?

A

executive dysfunction

  1. reduced verbal, nonverbal fluency
  2. perseveration
  3. abstraction impaired
  4. retrieval deficits
  5. poor set shifting
  6. poor strategies on copying tasks
  7. impaired attention
  8. depressed mood

i.e frontal lobe infarcts, penetrating head injuries as causes

171
Q

what is medial frontal syndrome?

A
  1. apathy/abulia (slowing of thinking) are the most consistent features
  2. lack of motivation and drive
  3. emotional emptiness/blunting
  4. failure to implement new plans
  5. poor performance and maintenance of output on fluency tasks
  6. decreased motor activity
  7. in extreme form, akinetic mutism (no initiation of speech or voluntary movements)

i.e ACA/MCA borderzone infarcts, ruptures ACA aneurysms, falx meningiomas, hydrocephalus

172
Q

define aphasia

A

an impairment of language produced by brain dysfunction

dont confuse with disorders of articulation (dysarthria), auditory disorders or psychiatric illnesses

173
Q

where is language primarily processed?

A

in the dominant hemisphere–> left is dominant in most right and left handed people

174
Q

where are the non verbal aspects of communication processed (i.e tone, prosody)?

A

non-dominant hemisphere–> usually right

175
Q

which is more anterior, broca’s area or wernickes?

A

brocas (wernicke’s is more posterior, at the end of the lateral sulcus)

176
Q

what are the examinable components of language?

A

speech

auditory comprehension

repetition

naming

writing

reading

177
Q

what aspects of speech can you examine?

A

articulation

fluency (rate and rhythm)

effort (time before you can speak)

word finding

paraphasias (word errors)

prosody (intonation and tone)

178
Q

what causes problems with speech articulation?

A

this is dysarthria, and it is not a language disorder per se….

can be due to UMN lesions, LMN lesions, neuromuscular junction lesions, cerebellar lesions, extrapyramidal lesions etc

179
Q

what suggests someone is having problems with word finding?

A

pauses in speech

180
Q

what are the types of paraphasias?

A
  1. phonemic (literal) paraphasias–> i.e sound substitution like “cable” instead of “table”
  2. semantic paraphasia–> word substitution i.e “hat” instead of “coat”; “seahorse” instead of “unicorn”
  3. neologisms–> made up words
181
Q

what type of lesion usually causes dysprosody or aprosody?

A

non-dominant hemisphere lesion

182
Q

what 3 steps are there in evaluating a language disorder (in order to classify it)?

A
  1. is the output fluent or nonfluent?
  2. is comprehension impaired or intact?
  3. is repetition impaired or intact?
183
Q

what type of aphasia has the following characteristics?

fluent, comprehension intact, repetition intact

A

anomic aphasia (only problem is naming)

184
Q

what type of aphasia has the following characteristics?

fluent, comprehension intact, repetition impaired

A

conduction aphasia

185
Q

what type of aphasia has the following characteristics?

fluent, comprehension impaired, repetition impaired

A

wernicke’s aphasia

186
Q

what type of aphasia has the following characteristics?

fluent, comprehension impaired, repetition intact

A

transcortical sensory aphasia

187
Q

what type of aphasia has the following characteristics?

non-fluent, comprehension intact, repetition intact

A

transcortical motor aphasia

188
Q

what type of aphasia has the following characteristics?

non-fluent, comprehension intact, repetition impaired

A

broca’s aphasia

189
Q

what type of aphasia has the following characteristics?

non-fluent, comprehension impaired, repetition intact

A

mixed transcortical aphasia

190
Q

what type of aphasia has the following characteristics?

non-fluent, comprehension impaired, repetition impaired

A

global aphasia

191
Q

describe the characteristics of fluent aphasias

A

normal or increased output

no extra effort

normal phrase length

function words more than content words (empty speech)

paraphasias common

192
Q

describe the characteristics of nonfluent aphasias

A

decreased output

extra effort

decreased phrase length

content words more than function words (agrammatic speech)

paraphrasias are rare

193
Q

describe the characteristics of global aphasia. what causes it?

A

“worst case scenario”

all components of language are affected

nonfluent/absent speech production, impaired comprehension, impaired repetition

usually due to damage to both broca’s and wernicke’s areas i.e a fairly widespread lesion

194
Q

describe the characteristics of mixed transcortical aphasia. what causes it?

A

tends to be more rare

nonfluent/absent speech production, with impaired comprehension but repetition intact

caused my damage to the areas the communicate with broca’s and wernicke’s but broca’s wernickes and arcuate fasciculus are spared

trouble with both speech production and with comprehension of instructions

195
Q

what are motor aphasias?

A

non-fluent aphasias with intact comprehension

i. e broca’s aphasia –> damage to broca’s area meaning repetition is impaired (nonfluent aphasia with intact comprehension and impaired repetition)
i. e transcortical motor aphasia–> damage to other areas of the frontal lobes that communicate with broca’s area–> repetition is preserved (nonfluent, with intact comprehension and repetition)

196
Q

what is the most common form of aphasia?

A

broca’s

197
Q

what are sensory aphasias?

A

fluent aphasias with impaired comprehension –> “empty” speech, made up words, paraphasias etc…

i. e wernicke’s aphasia–> due to damage to wernicke’s area (fluent, impaired comprehension, impaired repetition)
i. e transcortical sensory aphasia–> due to damage to other areas of the temporal/parietal lobes that communicate with wernicke’s area (fluent, impaired comprehension, repetition is preserved)

198
Q

what types of aphasias are fluent and have intact comprehension?

A

conduction aphasias

damage to areas affecting the arcuate nucleus

repetition is severely impaired

frequent paraphasias

i.e the woman who could not count to 10 in the video–> can follow commands but cant do repetitive/automatic verbal tasks

199
Q

if you have a patient with impaired writing without other language impairments, where is the lesion?

A

angular gyrus

200
Q

what is Gerstmann’s syndrome?

A

lesion to the inferior parietal lobule including the angular gyrus

4 components:
agraphia
acalculia
right/left disorientation
finger agnosia (inability to tell individual fingers apart)
201
Q

where is the lesion if your patient has alexia without agraphia? (cant read but can write)

A

lesion in left occipital cortex and posterior corpus callosum

(PCA)

information from the left visual field goes tot he right occipital lobe, and normally it should then cross over to the left angular gyrus and wernicke’s area to permit reading

an example of disconnection syndrome

202
Q

what apraxia?

A

loss of the ability to execute learned purposeful movements

NOT due to primary motor/sensory deficit–> comprehension, attention and motivation are intact

most apraxias are due to lesions in the DOMINANT hemisphere

203
Q

what is the most common form of apraxia?

A

ideomotor apraxia

failure to perform skilled/learned motor sequences on command or to imitation

i.e show me how you would brush your teeth/comb your hair

intent of the movement is usually still recognizable

204
Q

what is ideational apraxia?

A

conceptual deficit

difficulty in performing a sequence of steps to complete a task

loss of knowledge to select tools and objects

usually bilateral lobes are affected

205
Q

what is apraxia of speech?

A

difficulty translating motor plans into speech output–> but general buccofacial praxis is intact

speech is effortful but not due to an aphasia –> clue is that writin is intact

trial and error–> gropes for words

lesion is in dominant prefrontal areas near broca’s

difficulty wrapping their mouths around sounds; cant get the sound of the word quite right

206
Q

what is the most serious complication of cerebral angiography?

A

stroke

207
Q

what is one of the principle indications for using cerebra angiography?

A

in the investigation of patients with subarachnoid hemorrhage due to ruptured aneurysms

this is an excellent way to demonstrate the aneurysm and to also assess its suitability for either operative management or endovascular management with platinum coils

arteriovenous malformations are also bet evaluated using cerebral angiography

208
Q

what % of strokes are ischemic?

A

85%

50% of those are in the MCA distribution

209
Q

what is the most common artery to experience an ischemic stroke?

A

MCA

210
Q

what % of ischemic cerebral strokes are watershed infarctions?

A

5-10%

between territories of two major arteries

211
Q

how do watershed infarcts appear on imaging?

A

“rosary” pattern of deep WM infarcts

three or more lesions more than 2 mm in diameter arranged linearly and parallel to lateral ventricle, situated in centrum seminovale or corona radiata

212
Q

what are the 4 Ps of acute stroke imaging?

A

parenchyma

pipes

perfusion

penumbra

213
Q

what does a hyperdense MCA on CT indicate? (in the case of a stroke)

A

predicts higher thrombus burden and potential for poorer outcome

when you can see the lesion/thrombus on CT then there is less likelihood that the thrombus will melt with tPA alone–> if you dont treat it youll have a big problem

214
Q

what does the “dot” sign on CT indicate in the context of stroke?

A

corresponds to thrombus in distal branches of MCA (M2, M3)

215
Q

what % of people with cerebral hemispheric stroke get conjugate eye deviation (CED) and how is this useful?

A

20% get it

lateralizes to ipsilateral hemisphere with 93% PPV

improves sensitivity of assessment on NCCT

216
Q

what imaging modality is the best imaging of the brain?

A

MRI

vessel assessment via MRA

217
Q

what are some benefits to functional imaging in the context of stroke?

A
  1. determination of volume of tissue at risk
  2. vascular distribution of the ischemia
  3. determine core

B&B Part 2 (5 decks)

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