Cerebral Vascular Disease Flashcards

1
Q

The Three Principle Functions of the Brain

A
  1. REGULATE TONE or WAKING
    –Brain stem
    –If this is not working – patient is comatose
    Bilateral injury to brain stem (ascending reticulatinum system knocked out – wakens higher areas of the brain) = coma
  2. OBTAIN , PROCESS and STORE information
    - -99% of fibers are interneurons connecting one part of the brain to the other
    - -brain is very interactive
  3. PROGRAM, REGULATE, and VERIFY MENTAL ACTIVITY
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2
Q

Brain
Hierarchy of structures

3

A

PRIMARY AREA (=PROJECTION) receives sensory or produces motor output

  1. Primary sensory: Where sensory goes first in the brain
  2. Primary motor: primary area for motor output

SECONDARY AREA (=ASSOCIATION): incoming information is processed or motor programs are prepared

  1. Areas where info is processed
  2. Needed for brain function-acknowledge what something is, where, what it is doing
TERTIARY AREA (zones of overlapping): the latest systems of cerebral cortex. Most complex forms of mental activity
-------There is more overlap, most complex interactions occur here, Issues occur here
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3
Q

Hemispheric specialization

A

A. left hemispheric language dominant:
96% of right handed people and 70% of left handed dominant people

B. motor dominance is used to describe hemispheric specialization (dominance usually defined by motor dominance—the side where motor dominance is which is opposite

C. some functions are bilateral, many are dominated by one hemisphere

we can describe by hemisphere or by how they present in extremities:
—right handed person has left hemisphere dominant

—left CVA, right hemi: speech is affected

—if right handed and stroke to right hemisphere-non dominant hemisphere-speech may not be affected at all

people who were left handed used to be forced into right handed and may not have a dominant hemisphere

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4
Q

Clinical Example: Hemispheric Specialization

verbal stimuli come in bilaterally but perceived more strongly in right ear, left hemisphere to process verbal stimuli

Implication?

A

implication, a patient hard of hearing should receive at least one hearing aide in the RIGHT ear

“left ear advantage” for non verbal stimuli ie music, sounds, other nonverbal input

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5
Q

Primary motor area of Frontal Lobe

A
o	Brodmann’s #4
o	Complex, multijoint movements
o	Voluntary movements
o	Especially  hand control
o	If only this area of the brain is affected – fine motor movement is gone
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6
Q

Betz Cells

A
  • Come off of primary motor cortex
  • Cells that go to (monosynaptically) to the spinal cord level that they innervate

• Only involved in about 50% of movement
–other pathways involvd

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7
Q

FRONTAL LOBE

Primary motor area (brodman 4):

A

Primary motor area (brodman 4):
posterior part of frontal lobe-

  1. Complex multijoint movement
  2. Voluntary movements
  3. Especially hand control

–rare that only this alone affected but if it is only fine dexterity will be an issue

—primary betz cells (only 50% of movement) come off primary motor cortex and go directly monosynaptically to spinal cord level they innervate and are important motor cells—but they are only in 50% of movement and we have other pathways

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8
Q

FRONTAL LOBE

B. Premotor area:

A
  1. Postural sets before movements
  2. Visually guided movements –strong interaction with cerebellum
    - Control eye movements
  3. LESIONS—weakness, spasticity, motor apraxia

[online: Lesions of the premotor cortex lead to slowing of anticipated movements but do not lead to paralaysis

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9
Q

FRONTAL LOBE

C. Frontal eye fields

A
  1. Visual tracking, conjugate gaze-motor aspect of vision (vision in occipital lobe but motor aspect of vision is in frontal lobe)
  2. Coordination of bilateral UE tasks
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10
Q

FRONTAL LOBE

D. Broca’s area

A
  1. Motor aspect of speech
  2. Not needed for controlling mouth or tongue but to FORM WORDS AND SENTENCES -not the muscle activity of speech
  3. LESIONS:
    EXPRESSIVE APHASIA: one word at a time, words stuck on tip of tongue-not form fluency –know what want to say, can move mouth, cannot get it out
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11
Q

FRONTAL LOBE

E. Supplementary Motor area:

A

small area, midline in the brain, in front of frontal eye field, it is deep

  1. Initiation of movements
  2. Planning sequential movements
  3. Execution of these movements, especially INTERNALLY GENERATED
  4. LESIONS: poverty? of movement
    [online lesion to SMA inhibit the ability to perform complex movements]
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12
Q

Frontal Lobe Areas

A

A. Primary motor area (brodman 4):

B. Premotor area:

C. Frontal eye fields

D. Broca’s area

E. Supplementary Motor area:

F. All other areas: prefrontal cortex: personality, emotion, self initiation, impact upon others

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13
Q

Frontal lobe syndromes:

Post CVA: TBI etc.: need a separate rehab environment because of the psychological behavioral implications –may be aggressive, sexual advances

A

A. Dorsolateral lesions: apathy, lack of ability to plan or to sequence

  • –Poor memory for verbal information (If left hemisphere L)
  • –Or spatial information (if right hemisphere L)

B. Anterior lesion:

  • –response inhibition, difficulty with disinhibition, emotional lability, and memory disorders.
  • –Impulsiveness, sexual disinhibition, lack of concern for others
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14
Q

ONLINE

LESIONS TO FRONTAL LOBE

A

Primary motor cortex (area 4): Patient’s fingers lack precise coordination.
Patient cannot precisely contract just one digit or a particular group of digits.

Premotor cortex (lateral area 6): Patient cannot initiate the movement the patient
wishes to make. Patient exhibits motor apraxia (defect in motor performance without paralysis)
because the selection of a particular movement is impaired.

Supplementary motor area (medial area 6): Patient cannot tie shoe laces (impaired
selection of a particular movement sequence).

Parietal association: Patient has no sock on one foot because of sensory neglect.
Patient has ataxia (inaccurate movements)

Somatosensory cortex: Patient must look to sense where the hand is.
Loss of proprioception results in a reluctance to use affected limb.

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15
Q

FRONTAL LOBE

Dorsolateral lesions

A

apathy, lack of ability to plan or to sequence

  • –Poor memory for verbal information (If left hemisphere L)
  • –Or spatial information (if right hemisphere L)
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16
Q

FRONTAL LOBE

Anterior lesion:

A
  • –response inhibition, difficulty with disinhibition, emotional lability, and memory disorders.
  • –Impulsiveness, sexual disinhibition, lack of concern for others
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17
Q

PARIETAL LOBE

areas

A

A. Primary area: localize
Somatosensory areas

B. Secondary areas—interpretation:

C. Association areas: also need PNS to get the cortical sensation

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18
Q

PARIETAL LOBE

primary somatosensory cortical area

A

Somatosensory areas—brodman 3, 1, 2-posterior to primary motor area: what I feel and where

  1. Localization of touch, pain, temperature, and pressure
  2. Texture, shape and size
  3. Conscious proprioception

(peripheral issue cannot have this)

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19
Q

PARIETAL LOBE

Secondary areas

A

interpretation: it feels weird but it wont hurt me, interpretation is important (in stroke signals come but they don’t know how to make sense of it vs a peripheral issue)

Interpretation of sensation:

stereognosis

graphesthesia

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20
Q

Association areas:

A

also need PNS to get the cortical sensation

  1. Texture, size discrimination
  2. Same as secondary areas
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21
Q

Parietal Lobe syndromes (deficits if non-dominant right hemisphere is involved)

A

ie lesion in right hemisphere present with left hemiplegia

A. Left sided neglect:

B. Anosognosia:

C. Alexia:
D. Agraphia

E. Extinction of bilateral simultaneous stimulation

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22
Q

Left sided neglect:

A

Parietal Lobe syndromes (deficits if non-dominant right hemisphere is involved)

LESION IS IN RIGHT HEMISPHERE–LEFT SIDED NEGLECT (most people dominant in left hemisphere)

lack of recognition of left body parts (don’t know its there, don’t pay attention to it)

  1. ie hitting the wall on neglected side wheeling down hallway and think wc broken because don’t know hitting wall on that side
  2. tx: have family visit on that side of them, get them across midline, stand on that side, talk to them from that side because they will hear you, forced use to cross midline
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23
Q

Anosognosia:

A

Parietal Lobe syndromes (deficits if non-dominant right hemisphere is involved)

unaware of deficit, denial of disability

  1. They have denial of this deficit
  2. They are unaware of the deficit
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24
Q

Alexia

A

Parietal Lobe syndromes (deficits if non-dominant right hemisphere is involved)

inability to read

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25
Q

Agraphia

A

Parietal Lobe syndromes (deficits if non-dominant right hemisphere is involved)

inability to write
inability to calculate

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26
Q

Extinction of bilateral simultaneous stimulation:

A

Parietal Lobe syndromes (deficits if non-dominant right hemisphere is involved)

Extinction of bilateral simultaneous stimulation: only perceive stimuli on one side of the body

Stimulate on both sides but they only recognize the touch on the good side

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27
Q

Ideational Apraxia

A

Parietal Lobe syndromes (deficits if non-dominant right hemisphere is involved)

IDEATIONAL

  1. Inability to produce or describe motor tasks, patient cannot describe the task, even with cues or when given the object
  2. The engram cant be tapped for the task
    a. Often associated with dementia
    b. Gait apraxia
    c. Many ADL that cant be performed
  3. Ex: DRESSING APRAXIA: don’t know sequence of putting on a shirt, don’t have motor issue (ie of strength or tone) but they cannot sequence the task
  4. Ie cant sequence phases of walking in parkinson patient
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28
Q

Ideaomotor Apraxia

A

Parietal Lobe syndromes (deficits if non-dominant right hemisphere is involved)

 (most common)
  1. Inability to produce on command, purposeful movements
  2. Patients may be able to describe the task, but cant execute the motor task
  3. Has the idea but cannot execute serial steps for performance
    - Gait apraxia
    - Unable to perform many aspects of ADL
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29
Q

Agnosia:

A

inability to process one or more forms of the sensory information

—could also be a deficit and have difficulty with tactile cues (other cues they have)

—we want to at first compesate but we want them to relearn the task rather than compensate

1) TACTILE agnosia (asterognosis) (PARIETAL lobe lesion)

2) VISUAL agnosia-OCCIPITAL lobe
a. visual processing
b. putting it all together
c. they can hear it and put it together (ie someone walking down hall and we hear who it is) but not the auditory signal, not the written word

3) AUDITORY agnosia-TEMPORAL lobe

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30
Q

Temporal lobe and hearing

A

Auditory Cortex: sound localization (primary was to hear the sound, this is to make sense of where it is)

Unilateral lesion – minimal hearing loss —because auditory information is still coming in bilaterally

Bilateral lesion –deafness (rare)

Wernicke’s area: receptive, processing of speech, sounds—the reception of speech and processing of speech—processing of speech
(brocas was ability to form the words—word fluency, word finding)

***All other areas perception of all other sounds and auditory memory

(music is temporal lobe)

31
Q

Temporal Lobe Lesion: unilateral vs bilateral

A

Unilateral lesion – minimal hearing loss —because auditory information is still coming in bilaterally

Bilateral lesion –deafness (rare) (cortical deafness)

32
Q

Wernicke’s area:

A

Temporal Lobe
usually if stroke in dominant area ie LEFT

receptive, processing of speech, sounds—the reception of speech and processing of speech

—processing of speech
(brocas was ability to form the words—word fluency, word finding)

33
Q

Broca’s Area

A

FRONTAL LOBE
usually if stroke in dominant area ie LEFT

  1. Motor aspect of speech
  2. Not needed for controlling mouth or tongue but to FORM WORDS AND SENTENCES -not the muscle activity of speech
  3. LESIONS:

EXPRESSIVE APHASIA: one word at a time, words stuck on tip of tongue-not form fluency –know what want to say, can move mouth, cannot get it out

34
Q

If left handed person has stroke in L hemisphere:

A

non dominant for them, they are dominant in the right

If left handed has stroke in L hemisphere, perception things in non dominant hemisphere issue. Look at how each patient is presenting. Depends on what was dominant.

35
Q

Occipital Lobe and Vision:

A

rare involved in stroke,(because of vascularity)
occurs in TBI

  • *Primary visual cortex:
    1. SENSATION of light, shape, size, brightness
    2. Deficit: hemianopsia (decreased vision or blindness 1/2 visual field of one or both eyes)
  • *Association areas:
    1. Recognition.
    2. Visual attention, processing of visual information [Ie color, gaze, visual memory]

LESION: dominant hemisphere

  1. VISUAL AGNOSIA: deficit of visual recognition (visual agnosia)
    - –of faces: Someone with dementia may have this—not able to put image together of face and recognize the person
  2. OBJECT AGNOSIA-of objects
  3. VERBAL AGNOSIA-of words
    - –Word blindness
    - –Also called alexia
  4. Prosopagnosia: just unable to recognize faces

D. Bilateral lesions: cortical blindness (lesion in primary cortical area even if all other parts of vision are working, they are blind)

36
Q

Primary visual cortex:

A

occipital lobe

  1. sensation of light, shape, size, brightness
  2. Deficit: hemianopsia
37
Q

Association areas visual cortex of occipital lobe

A
  1. Recognition.
  2. Visual attention, processing of visual information
    Ie color, gaze, visual memory
38
Q

Lesion: dominant hemisphere of Occipital Lobe

A

Lesion: dominant hemisphere of Occipital Lobe

  1. Deficit of visual recognition (visual agnosia)
    - –Someone with dementia may have this—not able to put image together of face and recognize the person
  2. Of objects—OBJECT AGNOSIA
  3. Of words-VERBAL AGNOSIA
    - –Word blindness
    - –Also called alexia
  4. PROSOPAGNOSIA: just unable to recognize faces
39
Q

Bilateral lesions: Occipital Lobe

A

cortical blindness (lesion in primary cortical area even if all other parts of vision are working, they are blind)

40
Q

Prosopagnosia

A

face blindness,[1] is a cognitive disorder of face perception where the ability to recognize faces is impaired, while other aspects of visual processing (e.g., object discrimination) and intellectual functioning (e.g., decision making) remain intact.

lesion dominant hemisphere of Occipital Lobe

41
Q

VISUAL AGNOSIA:

A

deficit of visual recognition (visual agnosia)
—of faces: Someone with dementia may have this—not able to put image together of face and recognize the person

lesion dominant hemisphere of Occipital Lobe

42
Q

OBJECT AGNOSIA-

A

of objects

lesion dominant hemisphere of Occipital Lobe

43
Q

VERBAL AGNOSIA-

A

of words

  • –Word blindness
  • –Also called alexia

lesion dominant hemisphere of Occipital Lobe

44
Q

cortical blindness

what causes it

A

Occipital Lobe

Bilateral lesions: cortical blindness (lesion in primary cortical area even if all other parts of vision are working, they are blind)

45
Q

PART OF BRAIN

Finger movements

Counting out loud 1-20

Following a moving visual target

Listen to spoken words

A

Finger movements

  1. Motor cortex
  2. Supplementary motor cortex (upper anterior area)
  3. Premotor area
  4. Somatosensory area –constant feedback

Counting out loud 1-20

  1. Premotor area
  2. Broca’s area (inferior frontal)
  3. Wernicke’s area (superior temporal)
  4. Supplementary Motor Area (upper anterior frontal)

Following a moving visual target

  1. Visual association areas
  2. Supplementary motor area
  3. Frontal eye field

Listen to spoken words

  1. Auditory cortex: superior temporal gyrus
  2. Wernickes area: language comprehension
  3. Not motor areas because not producing speech
  • Note reading to themselves people tend to activate motor brocas
  • Lesion will affect function!!!
  • The corpus collosum needed to communicate between sides, if that is impaired the deficit will be the that the left brain doesn’t know what right brain is doing and visa versa
46
Q

name of structure connecting L and R brain

A

The corpus collosum

needed to communicate between sides, if that is impaired the deficit will be the that the left brain doesn’t know what right brain is doing and visa versa

47
Q

Finger movements

A
  1. Motor cortex
  2. Supplementary motor cortex (upper anterior area)
  3. Premotor area
  4. Somatosensory area –constant feedback
48
Q

Counting out loud 1-20

A
  1. Premotor area
  2. Broca’s area (inferior frontal)
  3. Wernicke’s area (superior temporal)
  4. Supplementary Motor Area (upper anterior frontal)
49
Q

Following a moving visual target

A
  1. Visual association areas
  2. Supplementary motor area
  3. Frontal eye field
50
Q

Listen to spoken words

A
  1. Auditory cortex: superior temporal gyrus
  2. Wernickes area: language comprehension
  3. Not motor areas because not producing speech
51
Q

Middle Cerebral Artery:

A

MOST COMMON SITE OF STROKE

  • –comes off the internal carotid
  • –supplying the insula and lateral surface of FRONTAL, PARIETAL, OCCIPITAL, and TEMPORAL lobes.

IN LESION: Posterior limb of the internal capsule is effected: thus blood flow more affected in UE than in LE

  1. Most common stroke is of the middle cerebral artery
  2. The UE > LE affected (internal capsule) in terms of blood flow
    - -stroke: better recovery in LE because of vascularity

Key is for HOW LONG: If not prolonged anoxia, less death of brain areas, of nerve damage

also was it a main vessel

52
Q

Dominant middle cerebral artery:

What do we see clinically (6)

A

1) Contralateral hemiplegia with UE more involved than the LE and face.
2) Distally greater than proximally
3) Aphasia: expressive or receptive. The more severe the aphasia, the larger the lesion, and usually the more severe the hemiparesis
4) Hononymous Hemianopsia: damage to optic radiations
5) One sided sensory deficit
6) if there is a small internal capsule infarct—pure motor deficit

53
Q

Anterior cerebral artery:

What do we see clinically (4)

A

medial surface of FRONTAL and PARIETAL lobes including anterior and genu of the internal capsule

less common
LOWER MORE THAN UPPER

  1. Hemiplegia with LE > UE involvement
  2. Mild aphasia secondary to damage to supplementary motor cortex (less of this anterior cerebral artery feeds to broca and wernickes area)
  3. Mental changes, loss of inhibition

(good therapy session and suddenly start crying)
(need to be safety aware with these patients and anyone with frontal lobe involvement, they may get up and fall if left alone)

  1. Some sensory deficit in LE
54
Q

Posterior Cerebral Artery:

A

less common
medial and inferior aspects of temporal and occipital lobes. Thalamic branches.

can involve corpus collosum

  1. thalamus:
    * **THALAMIC PAIN: persistent pain: If it hits the thalamus it is called thalamic pain because thalamus is central station for sensory input and lesion there will cause the thalamic pain from the damage in the sensory station in the brain, hard to manage

—impair superficial touch and deep sensation

  1. Occipital:
    Homonymous hemianopsia
  2. Dominant hemisphere and CORPUS COLLOSUM

***ALEXIA

***ANOMIA FOR COLORS [disconnect right occipital vision from left language]

  1. due to sensory deficit or motor tract involvement:
    ataxia
    tremor
55
Q

Internal Carotid Artery:

A

occlusion may be SILENT or it may cause MASSIVE cerebral infarct, damage most often occurs in the distribution of the MCA,

may include hemianopsia and retinal blindness.

IMPLICATION:
Minimal deficit: patient develops collateral circulation so serious blockage and minimal deficit if forming over many many years.

Severe deficit: sudden embolism blockage—more severe manifestation

56
Q

Interference

A
  • Name the color of the font of each work
  • When you look at one of the words, you see both its color and its meaning

o You have to determine which is more important

57
Q

Slope of severity of initial deficits and functional outcome

Motor deficit:

Motor and sensory deficit:

Motor, sensory and visual deficit:

A

Severity of initial deficits and functional outcomes (everyone is different)

  1. Graph
  2. Probability of achieving ambulation vs weeks post CVA

A) Motor deficit: greatest slope of recovery –recovery of motor unit recruitment, depends on damage and cause—hemoragic stroke is worse than embolism even in same area—bleeding and pressure on brain is worse than blockage

B) Motor and sensory deficit: slow recovery but wont prevent it without the sensory feedback or a neglect on a side, they can still get there but it is a harder and longer road

C) Motor, sensory and visual deficit: this has the most severe impact on an individual, don’t have the body awareness etc.

***It all depends on the patient: ie motivation, depression, comorbidities

58
Q

Higher cerebral dysfunction aphasia:

expressive aphasia

receptive aphasia

conduction

global

A

—-see communication disorders handout in course manual

  1. Expressive: Broca’s (frontal: understand, have trouble fluently forming words)
  2. Receptive: Wernicke’s (temporal lobe: word salad)
  3. Conduction—pathway between Broca and Wernickes’s effected
    —talk fluently but interpreting it isnt, they also may have a deficit where present more like receptive and fluent mixed vs receptive of mixed words but in some recovery can communicate with speech but slow and labored
  4. Global
59
Q

Severity of initial deficits and functional outcomes

motor

motor and sensory

motor, sensory, and visual

A

• Based upon how they present, what are some reasonable goals
• Probability of achieving ambulation vs. weeks post CVA
o Varies based on severity of stroke, the cause (hemorrhagic vs. embolus)

• If someone only has a motor deficit – greatest slope of recovery
o Can probably get recovery of motor unit recruitment

• Motor and sensory deficit – sensation will slow down recovery but doesn’t completely deter
o Have to overcome the sensory deficit before getting motor function – what slows the process

• Motor, sensory, visual – takes the longest to recover
o Don’t have the ability to compensate with visual

• Also have to take into account their level of motivation, co-morbidities to determine their prognosis (functional outcomes)

60
Q

movie

broca’s aphasia

A

• First picture is broca’s aphasia (expressive aphasia)
o How fluent is my speech
o They understand what you’re saying and what they want to say, just cant say it
o May have a word finding problem – say a similar word but not the same
• Overall you can understand their speech

we can use nondominant hemisphere music to help

61
Q

movie

wernicke’s aphasia

A

• Second picture is wernicke’s aphasia (receptive aphasia)
o Fluency and comprehending what you’re saying
o Words are coming out but they don’t make sense
o Word salad

62
Q

female with conduction aphasia

A

she understands questions but she cannot produce meaningful speech

63
Q

Dysarthria

structures involved?
synonym?
characteristics?
comprehend spoken speech?
speak fluently ?
produce meaningful language? 
normal grammatical use of words?
read?
write?
A

1) LMN or corticobulbar neurons
2) lack of motor control of speech muscles
3) comprehends spoken speech
4) does not speak fluently
5) produces meaningful language but difficult to understand
6) normal use of grammatical words
7) reads
8) writes

64
Q

Expressive Aphasia

structures involved?
synonym?
characteristics?
comprehend spoken speech?
speak fluently ?
produce meaningful language? 
normal grammatical use of words?
read?
write?
A

1) BROCA (usually left)
2) motor, expressive aphasia, NONFLUENT aphasia
3) grammatical omissions, errors, short phrases, effortful speech
4) UNDERSTAND spoken speech
5) DOES NOT speak fluently
6) produces meaningful language BUT GRAMMATICAL WORDS MISSING
7) NOT grammatical use of words
8) READS
9) DOES NOT write

65
Q

Receptive Aphasia

structures involved?
synonym?
characteristics?
comprehend spoken speech?
speak fluently ?
produce meaningful language? 
normal grammatical use of words?
read?
write?
A

1) WERNICKE’s area (usually left)
2) sensory, receptive or fluent aphasia

3) cannot understand language,
speak FLUENT
but UNINTELLIGIBLE

4) DOES NOT understand spoken speech
5) DOES speak fluently
6) DOES NOT produce meaningful language
7) DOES NOT HAVE normal grammatical use of words
8) CANNOT read
9) CANNOT write

66
Q

Conduction Aphasia

structures involved?
synonym?
characteristics?
comprehend spoken speech?
speak fluently ?
produce meaningful language? 
normal grammatical use of words?
read?
write?
A

1) NEURON’s CONNECTING WERINICKE’S WITH BROCA’S AREAS
2) DISCONNECTION APHASIA

3) UNDERSTANDS language but
LANGUAGE OUTPUT IS NOT INTELLIGIBLE

4) DOES understand spoken speech
5) DOES speak fluently
6) DOES NOT produce meaningful language
7) DOES NOT HAVE normal grammatical use of words
8) READS
9) CANNOT write

woman in video:
therapy: nonverbal communication, hand signals,

67
Q

Global Aphasia

structures involved?
synonym?
characteristics?
comprehend spoken speech?
speak fluently ?
produce meaningful language? 
normal grammatical use of words?
read?
write?
A

1) WERNICKE’s area, BROCA’s area, and the intervening cortical and subcortical areas
2) TOTAL APHASIA
3) cannot speak fluently, cannot communicate verbally
4) cannot comprehend spoken speech
5) cannot speak fluently
6) cannot produce meaningful language
7) cannot use normal grammatical use of words
8) cannot read
9) cannot write

68
Q

Neuroplasticity vs Localization

A
  • Localization is an anatomical guideline for brain function maturation
  • Research greatly and totally supports CSN reorganization for function. This includes restarting brain maturation that my have shut off prematurely
  • Consider the brain as an active learner. If no input (damaged pathways, bored), an area will begin to process other inputs, with proper training (remapping)
  • Neuron’s that fire together get wired together
  • —Axon’s enlarge, synapses increase and patterns emerge from practice
  • Engrams –patterns of brain function, areas that get fired together, their synapses have lesser threshold of firing

• Pathways get reorganized to restore function-Because the body is after total efficiency

69
Q

Phantom limb studies by Dr. Ramachandran:

A
  1. When the face is touched of a patient whose hand had been amputated, the person felt the sensation on his face AND on his “phantom” fingers
  2. Sensory areas in the brain are not being use (motor or sensory pathways) – they will change from disuse: motor pathways to that hand will atrophy, the sensory pathways are not being used, they will change from disuse. May take up other functions.
    a. Ie in a deaf person, other senses are heightened
    b. When face touched he felt sensation in his face and phantom fingers, and the same effect happened when he touched their arm: the arm’s sensory fibers had invaded the space that had been previously used by the hand = plasticity
  3. Remapping CNS: retrain an area of the brain to function in a different capacity : get it to interpret input in another way
    a. Remapping the sensory distribution of the tongue to replace vestibular dysfunction, using a motion sensor on the head for input

b. Remapping the tactile areas of the hand to see
c. Remapping occipital lobe for other sensory inputs in the blind
d. The brain is what interprets sensory information, and if unused by one sense, takes on other sensory processing

70
Q

Laterality Reconstruction

A

– restoring the brain’s concept of left and right extremities using pictures showing the left and right and bombarding appopriate information to help brain interpret better

71
Q

Visual and Motor Imagery

A

– Thinking about, then moving the involved extremity –think about and mentally review the movement activates the motor neurons of that movement without even any movement

72
Q

Mirror therapy

A

– the brain is tricked into thinking that the limb is better than it really is : Use mirror box: looking at the good side in the mirror to get the involved side to improve because brain thinks it is better than it is on the involved side (complex regional pain syndrome 1 or reflex sympathetic dystrophy)

73
Q

Neuroplasticity vs Localization: Research

A

A. Research has shown specific pre-language and training
B. Children with deficits in speech recognition, speed of decoding, etc greatly improved with specific retraining called “FastForward” software developed by a team of CNS researchers

74
Q

AUTISM

A

Possible early shutting down of critical periods of brain development

A. BRAIN DERIVED NEUROTRIPHIC FACTORS: BDNF: flood the brain and result in all brain connections becoming “important”

B. Massive myelination occurs but the brain cannot differentiate input and becomes hypersensitive to all input (SENSORY OVERLOAD)

C. This undifferentiated brain results in OVE ACTIVITY of large areas of the brain with any input (auditory, sensory, etc)

–BRAIN CANNOT PROCESS THIS OVERLOAD AND SHUTS DOWN

Research revealed ways to reopen the plastic, critical periods of brain differentiation and retain them to function normally