Aphasia Test 1

Front 1

Stroke is ____ leading cause of death in the US.

Back 1

3rd

Front 2

Risk Factors of Stroke

Back 2

Heart Disease
Diabetes
Smoking
Obesity
Birth Control Pills
Being a Male
Being African American
Having a family history of CVA.
If you have previously suffered a stroke or TIA.

Front 3

Heart Disease as a risk factor for stroke

Back 3

High blood pressure
coronary artery disease
high cholesterol

Front 4

Diabetes as a risk factor for stroke

Back 4

Diabetes causes high glucose levels, which results in fatty deposits on your arteries.

Front 5

Smoking as a risk factor for stroke

Back 5

reduced oxygen in blood from nicotine
high blood pressure
cholesterol deposits form on artery walls from carbon monoxide

Front 6

Obesity as a risk factor for stroke

Back 6

places strain on your heart and blood vessels
associated with high blood pressure and diabetes

Front 7

Birth control pills as a risk factor for stroke

Back 7

increased ocurrence of blood clots
increase if over 30 yrs old
increase if take BCP and smoke together

Front 8

Rostral/Caudal

Back 8

towards head/towards tail

Front 9

ventral/dorsal

Back 9

towards front/towards back

Front 10

Frontal Lobe boundaries

Back 10

posterior: central sulcus
inferior: lateral sulcus

Front 11

Frontal lobe makes up ____ of the surface of each hemisphere.

Back 11

1/3

Front 12

Frontal Lobe Structures of Interest

Back 12

Precentral gyrus

Front 13

Precentral Gyrus
AKA/function

Back 13

primary motor strip/Area 4
voluntary control of skeletal mms on the contralateral side

Front 14

premotor area
AKA/function

Back 14

Area 6
planning and intitiating sequential, volitional mvmt

Front 15

gyri/sulcus

Back 15

hills/valleys

Front 16

sagittal cut

Back 16

divides left and right

Front 17

horizontal/transverse cuts

Back 17

divides top and bottom

Front 18

coronal cut

Back 18

dives front and back

Front 19

Parietal Lobe Boundaries

Back 19

anterior- postcentral gyrus
posterior- undefined
inferior- lateral sulcus

Front 20

Postcentral gyrus
AKA/functions

Back 20

AKA primary sensory strip/1,2,3
receives sensations of touch and pressure (but not pain and temp)

Front 21

Temporal Lobe
AKA/Functions

Back 21

perception/processing of auditory information
Left- comprehending verbal and written material, process meaning and syntax
Right- processing nonverbal visual info and nonverbal sound

Front 22

Temporal Lobe Boundaries

Back 22

superior- lateral sulcus
inferior- on underside of hemisphere
posterior- undefined

Front 23

Temporal Lobe Structures of Interest

Back 23

Superior temporal gyrus (22)
middle temporal gyrus (21)
inferior temporal gyrus (20)
Heschl's gyrus (41, 42)
Wernicke's area (22)
posterior portion of the lateral sulcus

Front 24

Parietal Lobe Structures of Interest

Back 24

Postcentral gyrus (1, 2, 3)
supramarginal gyrus (40)
angular gyrus (39)

Front 25

Occipital Lobe
Boundaries, structures of interest

Back 25

No clear boundaries
Primary visual cortex (17)
Primary visual association area (18, 19)

Front 26

Association Cortex

Back 26

fibers that run amongst all areas within a hemisphere, they interpret information and provide meaning

Front 27

damage to association cortex but spared primary areas causes_____

Back 27

agnosia

Front 28

A large group of fibers can be a ____1___. A large ____1__ can be a __2_____.

Back 28

bundle
fascicululous

Front 29

arcuate fasciculus

Back 29

connects wernicke's area to broca's area (does not cross lateral sulcus, arcs around) used to process and interpret information.

Front 30

damage to arcuate fasciculous

Back 30

breaks connections between broca's and wernicke's, but both work separately. will NOT be able to repeat and have difficulty monitoring speech (speech will contain paraphasic errors)

Front 31

pre-frontal area (tertiary cortex)

Back 31

involved with personality, expression of emotion, drive/ability to inhibit, helps us set goals, solve problems, plan

Front 32

lower/medial portions of temporal lobe (tertiary area)

Back 32

episodic memory, recalling words

Front 33

Commissural fiber

Back 33

corpus callosum
runs between hemispheres

Front 34

anterior cerebral artery supplies _____

Back 34

medial surface of cortex from the frontal lobe all the way to the temporal-parietal-occipital sulcus

Front 35

if anterior cerebral artery is occluded __________results

Back 35

motor impairment, may have trouble with EF

Front 36

MCA supplies blood to _____

Back 36

entire lateral hemisphere, including all 4 lobes.

Front 37

aphasia results from damage to ____

Back 37

MCA!

Front 38

the brain is fed by two main arteries:

Back 38

common carotid and vertebral

Front 39

internal carotid forms the ___ and ____

Back 39

MCA and anterior cerebral artery

Front 40

the vertebral artery goes through the ____ and forms the _____ artery

Back 40

vertebral column, basilar artery

Front 41

the basilar artery divides into ___ and ____

Back 41

left and right posterior cerebral arteries

Front 42

ant comm artery connects the _____

Back 42

left and right ant cerebral arteries.

Front 43

the post comm artery connects the ____

Back 43

basilar/PCA juncture to the internal carotid just before it divides

Front 44

Disruption of the ant cerebral artery causes

Back 44

impaired motor strip, leading to paralysis of legs and feet, and or prefrontal areas, leading to impairments in EF

Front 45

disruption of posterior cerebral artery causes

Back 45

visual field blindness (feeds occipital lobe and inferior/lateral portions of the parietal lobe)

Front 46

watershed areas

Back 46

the ends of the ant cerebral artery, post cerebral artery, MCA connect with each other. the area in which this connection occurs is referred to as watershed area. this connections provides another source of collateral circulation where blood from one artery could flow into another if needed.

Front 47

right homonymous hemianopsia

Back 47

Since the primary visual area in one hemisphere receives sight from the opposite half visual field, damage to the left primary visual area will cause blindness in the right half of the visual field.

Front 48

motor root of spinal nerves

Back 48

aka ventral root. in anterior portion of spinal cord.

Front 49

sensory root of spinal nerves

Back 49

aka dorsal root. in posterior portion of spinal cord.

Front 50

two tracts from spinal nerves are ___ and ___

Back 50

pyramidal and extrapyramidal tracts

Front 51

primary motor strip/precentral gyrus is in charge of controlling all ______ movement on ______ side of body

Back 51

voluntary, contralateral

Front 52

_____ is origin of pyramidal tract

Back 52

precentral gyrus

Front 53

pyramidal tract course

Back 53

down brain, through internal capsule, through pons, to brainstem, connects with cranial nerves, courses down spinal column, connects with spinal nerves

Front 54

_____is where pyramidal tract synapses with ventral/motor root of spinal nerves

Back 54

final common pathway aka direct activation pathway

Front 55

__________ tract is direct pathway to initiate all skilled, voluntary movement

Back 55

pyramidal tract

Front 56

______________ is indirect activation pathway. it originates in ______

Back 56

extrapyramidal, BG

Front 57

function of extrapyramidal tract

Back 57

adjust mm tone and posture during volitional movement

Front 58

sensory info travels from post. horn of spinal cord through ____ and into post central gyrus

Back 58

thalamus

Front 59

stroke aka cva aka brain attack

Back 59

sudden onset of prominent and usually persistent neurological deficit

Front 60

warning signs of stroke

Back 60

FAST
F- droopy face
a- arms drifts to ground
s- slurred speech
t- no time to waste

Front 61

most common type of stroke

Back 61

ischemic (75-80%)

Front 62

what happens during ischemic stroke

Back 62

as blood flow reduces, brain does not get enough oxygen and glucose. if that continues, necrosis occurs and then an infarct

Front 63

within 24 hrs of stroke

Back 63

the brain does not respond. there is an initial onset of a stroke and sometimes the stroke continues. Stroke many continue for several hours (evolving/progressive stroke).

Front 64

3-5 days after stroke

Back 64

the brain is swelling, full of fluid in tissues, edema, will reach its maximum swelling point.

Front 65

7th day of stroke

Back 65

the swelling and edema start to diminish,

Front 66

12-21 days after stroke

Back 66

the swelling and edema should be resolved. The brain works to heal itself.

Front 67

one month after stroke

Back 67

brain starts to reabsorb dead tissue (this continues for a few months). A cavity is left (depending on how much tissue has died), and the cavity will be filled with fluid. Sometime atrophy from aging has more dramatic effect because of cavity.

Front 68

hemorrhagic stroke

Back 68

16% of strokes, Results from bleeding from an artery in the intracranial space.

Front 69

3 causes of hemorrhagic stroke

Back 69

• Rupture of a blood vessel which causes hematoma
• Rupture of aneurysm (ballooning/bulging of weakened blood vessel).
• An AV Malformation (Arterial Venous Malformation), which is congenital (you may not know you have it until it bleeds. If AVM, it is very challenging to stop bleeding but allow for adequate blood flow.

Front 70

3 ares of occurence in hemorrhagic stroke

Back 70

• Within the working part of the brain, which is deep in our cortex, The BG
• Subarachnoid space (almost always because of an aneurysm). The aneurysms are almost always at the base of the brain on the vertebral arteries.
• Subdural space

Front 71

damage from hemorrhagic stroke

Back 71

• Increased pressure to the area of the brain where the blood is flowing.
• If you can stop the bleeding and relive the pressure, function returns. You’re much more likely to die from a hemorrhagic stroke. If you survive, you have less functional impairment than if you survive an ischemic stroke.

Front 72

TIA

Back 72

• A brief, focal, cerebral event. The symptoms develop quickly and they leave within 2 minutes-24 hours.

Front 73

symptoms of TIA

Back 73

motor dysfunction (lack of movement or weakness in limbs), sensory changes (numbness or tingling in face or extremities), gait/posture abnormalities (can’t sit straight in a chair), double vision, brief dysarthria, brief dysphagia, dizziness (but is always associated with another symptom).

Front 74

symptoms of PPA

Back 74

range of impairments in comprehension, naming, speech fluency, reading, writing

Front 75

focal neurological signs of a stroke

Back 75

• May see paralysis on one side of the body, speech production/comprehension problems, memory loss, confusion, and sensory impairment.

Front 76

why do strokes occur?

Back 76

• The blood vessels in our brain are frailer and not as thick as the rest of the blood vessels in our body. They react to differences in blood pressure, chemical changes in our blood, and they do so more quickly, react stronger than the rest of our body. It is easier for the vessels in our brain to rupture.

Front 77

CT strength/weakness

Back 77

cross-sectional images of brain taken from various angles to ID presence/location of lesion. radiation exposure. affordable but does not allow immediate visualization

Front 78

MRI strength/weakness

Back 78

 Look at brain’s ability to utilize glucose for feeding nerve tissue. Examine areas that are more/less active. Very expensive, mostly used for research purposes.

Front 79

fmRI strenghts/weakness

Back 79

 Show more structure than PET. Can see ventricle, have some sense of position and shape of cerebrum, the fMRI is analyzing blood flow. Look at highly oxygenated blood verses less oxygenated blood. Look at color and intensity of blood. Will be able to pinpoint area of thrombosis or hemorrhage if see area of less oxygenated blood.

Front 80

corticospinal tract (pyramidal tract)

Back 80

• Starts on primary motor strip in each hemisphere. Connects primary motor strip to spinal nerves, which travel to our limbs. Courses down through brain, at level of medulla, it decussates.

Front 81

lesion to corticospinal tract

Back 81

If you have a lesion on the corticospinal tract above the level of decussation, you are going to have contralateral weakness or paralysis. If lesion occurs below level of decussation, clinical signs will be ipsilateral.

Front 82

corticobulbar tract (pyramidal tract)

Back 82

• Starts on precentral gyrus (primary motor strip). Connects to the cranial nerves. Provides innervation to the head and neck ipsilaterally and contralaterally.

Front 83

exceptions to bilateral lesions of corticobulbar tract

Back 83

hypoglossal nerve and the facial nerve

Front 84

lesions to corticobulbar tract

Back 84

see google doc

Front 85

apraxia

Back 85

motor speech disorder/impairment in the motor programming of volitional speech movements/loss of voluntary control of speech production.

Front 86

dysarthria

Back 86

motor speech disorder/impairment in the execution of speech movement due to mm weakness, slowness, or discoordination. Dysarthric speech may sound slurred, hoarse/harsh/strained voice, decreased breath support.

Front 87

auditory agnosia

Back 87

impaired processing of all auditory information including environmental sounds (phones, baby crying, sirens)

Front 88

auditory verbal agnosia

Back 88

-(pure word deafness)- because of site of lesion, patient can’t understand language that they hear, but can talk, write, and read ok.

Front 89

visual-verbal agnosia

Back 89

(pure word blindness, pure alexia)- can’t read but can talk, listen, and write

Front 90

paraphasic errors

Back 90

patients after stroke do paraphasic errors at a pathological level. Types of errors they have helps us to know what kind of aphasia they have

Front 91

types of paraphasic errors

Back 91

verbal
semantic
phonemic (literal)
phonic (formal)
neologisms
jargon

Front 92

verbal paraphasic errors

Back 92

unrelated real word substitution (pencil/dog)

Front 93

semantic paraphasic error

Back 93

related word substitution (cat/dog)

Front 94

phonemic (literal) paraphasic error

Back 94

sound substitution (pog/dog, spork/fork)

Front 95

phonic (formal) paraphasic error

Back 95

whole word substitution that shares phonemes with target (pickle/player)

Front 96

neologism paraphasic error

Back 96

nonwords which may or may not have a resemblance to target

Front 97

jargon paraphasic error

Back 97

most words, even function words, are replaced with non-words.

Front 98

2 controversies of aphasia

Back 98

can you classify it? is there more than 1 type?

Front 99

4 viewpoints

Back 99

general language disorder
pieces/parts language disorder
impaired access
psycholinguistic/cognitive

Front 100

general language disorder (viewpoint)

Back 100

• A language impairment in all areas (even reading, writing, speaking, listening)
• No other impairment. Aphasia is a pure language impairment.
• If a patient had difficulty with reading and writing could could listen and speak, they do not have aphasia.
• Hildred Schuell and Fred Darly associated with this viewpoint.

Front 101

pieces/parts viewpoint

Back 101

• From Boston School, Goodglass and Kaplin (authors of Boston Diagnostic Aphasia Examination and Western Battery are based on this viewpoint).
• Is a wildly popular viewpoint.
• Various modalities of language can be selectively impaired and called aphasia. If you know the clinical area that is impaired, you can make a hypothesis to what area of the brain is damaged. Relationship between anatomical site of lesion and clinical function. (Remember aphasia must be from a CVA)

Front 102

impaired access viewpoint

Back 102

• Doctor McNeil- University of Pennsylvania
• Not widely accepted
• Language is not primary impairment. What’s impaired is patient’s ability to access it. Physiologically, their brain is not allowing them to get to language stored in the brain because of changes that have occurred from CVA. Decreased reaction time, increased sensory threshold, attention fluctuates, can’t allocate as much effort to understanding, get tired easily. Aphasia would not be addressed, changes would be addressed.

Front 103

pyscholinguistic/cognitive viewpoint

Back 103

• Clarke and Murray, Dr. Chapey (Arizona)
• Aphasia is an acquired impairment in language and the cognitive processes that underlie it. Aphasia impacts all modalities of language and cognition (memory/attention may be impaired).

Front 104

definition of aphasia

Back 104

• A language impairment resulting from a stroke. It is characterized by impairment in all language modalities including speaking, listening, reading, and writing but not necessarily to the same degree in each modality. Aphasia may be accompanied but not required to be accompanied by impairment in memory and higher cortical functioning.

Front 105

be able to draw pictures and label parts!

Back 105

!

Front 106

explain homonymous hemianopsia

Back 106

!

Front 107

draw circle of willis

Back 107

!

Front 108

know Brodman's areas

Back 108

!

Front 109

If a person had a lesion to the corticobulbar and corticospinal tracts of the left hemisphere the result would be:

Back 109

1. Right hemiparesis/paralysis
2. Right facial weakness
3. Deviation of the tongue (this may be transient)