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MedCon Rehab II > COMPS:CVA Part II: Focus on CVA EXAM 1 > Flashcards

COMPS:CVA Part II: Focus on CVA EXAM 1 Flashcards

1
Q

Middle Cerebral Artery

A

In relation to Circle of Willis

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2
Q

MCA

A

Lat. Surface of the Brain

UE’s

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3
Q

MCA occlusions are generally MORE ________ than ________

A

MORE Embolic

*Clot from Somewhere else in body travels to brain

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4
Q

MCA is the most often occluded artery as a result of:

A

Vascular disease

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5
Q

MCA supplies:

*Most often occluded artery*

A

Lateral surface of the brain (UE’s according to Homonculus)

BG

portions of Internal Capsule

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6
Q

MCA Occlusion: what are the results?

A

Results in:

  • ALL Contralateral (opp. side)
    • ​contralat spastic hemiparesis
    • contralat hemianesthesia
    • contralat homonymous hemianopsia
      • ==> impaiment in conjugate gaze in direction opp the lesion​
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7
Q

Explain Contralateral hemianopsia in MCA occlusions

A
  • Impairment in Conjugate gaze (keeping eyes focused together on target)
    • In direction OPP the lesion
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8
Q

W/ MCA occlusion: what happens if L hemisphere involved

AND is the language dominant side?

A
  • Global Aphasia
    • Expressive and receptive communication disorder
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9
Q

W/ MCA occlusion: what happens if R hemisphere affected?

A
  • Anosagnosia–> denial of illness or lack awareness of problem
    • ​W/OUT Aphasia
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10
Q

UPPER division of MCA occlusion

A
  • NON-Fluent Broca’s - Oromotor aphasia
    • ​seen w/ hemiparesis in face and UE MORE than LE
      • ​bc MCA is UE’s (lateral brain)
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11
Q

UPPER division MCA occlusion

Broca’s Oromotor aphasia

Called this….

A

Brachial Syndrome

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12
Q

Broca’s area affected (UPPER division MCA) === Broca’s aphasia

which is what?

A

Non-fluent, expressive problem

NOTE: comprehension is OK

NOTE: have trouble w/ MOTOR output of speech

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13
Q

INFERIOR Division MCA occlusion: Dominant side (language side)

A

Wernicke’s aphasia w/out hemiparesis

arm/leg sparred

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14
Q

Broca’s aphasia (UPPER division MCA) you WILL see

A

hemiparesis face and UE

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15
Q

INFERIOR division MCA occlusion (Wernicke’s aphasia) you will NOT see

A

hemiparesis

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16
Q

Wernicke’s Aphasia W/out hemiparesis…

Likely findings Associated w/…

A
  • Hearing intact, auditory COMPREHENSION lost
  • Alexia (unable to read) Agraphia (unable to write)
  • distortion of articulate speech
  • Hearing intact
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17
Q

Wernicke’s Aphasia w/out hemiparesis

Describe the speech

*remember comprehension lost

*remember word salad

A
  • Speech is Fluent w/ natural language rhythm, BUT
    • ​has neither understandable meaning nor syntax
  • ​​**Despite loss of comprehension, word memory is preserved and words are often chosen correctly
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18
Q

What TYPE of Aphasia is Wernicke’s ?

A

Expressive, Fluent aphasia

*person may speak fluently w/ natural rhythm, but result has neither understandable meaning nor syntax

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19
Q

INFERIOR division MCA occlusion: NON-dominant side (non-language side)

yields:

A
  • PURE hemiplegia (half paralysis) OR
  • spatial agnosia (hemineglect) WITHOUT weakness
    • ​lose sensory function on that side AND proprio. awareness
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20
Q

ACA

A

In relation to Circle of Willis

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21
Q

ACA

LE’s!!! Middle of homonculus

A

Brain region covered

LE’s

Middle of homonculus

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22
Q

ACA syndrome occurs due to _______ MORE than __________ and is __________

A

Occurs due to Embolism (moves around) MORE than thrombus

RARE!!!

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23
Q

Why is ACA syndrome frequently asymptomatic?

A

Good collateral circulation

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24
Q

W/ ACA syndrome: If the Dominant Language side is affected:

what happens ?

A
  • Abuila
    • inability to make decision
  • reduction in rate and complexity of speech
    • aka scanning speech—> pauses b/w words
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25
Q

ACA syndrome: Dominant language side

whats affected limb wise and result wise?

A

Contralateral LE > UE

paresis and sensory loss

remember ACA is medial side homonculus==> LE

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26
Q

Internal Carotid Artery syndrome can be due to 3 things:

A
  1. Hypoperfusion
  2. Embolus–moves around
  3. Thrombus–blockage in one place
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27
Q

Frequently an accompanying symptom of ICA syndrome

why??

A
  • Transient MONocular blindness
    • aka amaurosis fugax
    • bc ICA supplies Opthalmic artery
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28
Q

Explain Transiet monocular blindness

sx ICA syndrome

A
  • Temp. fading of vision or blindness
    • mins—> days
  • due to DEC blood supply from ICA to opthalmic artery
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29
Q

ICA is very close in proximity to MCA

what does this mean?

A

IC occlusion often results in MCA syndrome

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30
Q

w/ an ICA syndrome,

COMPLETE blockage w/out adequate collateral circulation results in what?

A
  • deficits in both MCA and ACA
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31
Q

PCA

A

in relation to Circle of Willis

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32
Q

PCA syndrome: Central occlusion

most affected areas?

A
  • Subthalamus
  • Medial thalamus
  • Ipsilateral (same side) cerebral peduncle
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33
Q

PCA distribution

A

In brain…

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34
Q

Proximal PCA syndromes

Where in the brain would this occur?

A

See pic!!!

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35
Q

3 results from Proximal PCA Syndromes

A
  1. Thalamic pain syndrome
  2. Contralateral hemiplegia from cerebral peduncle involve.
  3. Hemiballismus
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36
Q

Typified by 1 month recovery from hemisensory loss

followed by BRUTAL, intractable PAIN

A

Thalamic pain syndrome

*Proximal PCA syndrome

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37
Q

transition FROM BS to cortex

*similar to ICA or MCA stroke

indicates involvement where and for what syndrome?

A

Contralateral hemiplegia from cerebal peduncle involve.

*Proximal PCA syndrome

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38
Q

LOSE ballistic mvmts 1/2 side

typified by flinging, flailing mvmts of ONE extremity

subthalamic nuceli infarct

A

Hemiballismus

*Proximal PCA syndrome

*Subthalamic nuclei infarct —-THINK PCA

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39
Q

Peripheral PCA syndromes

problems typically_________

A

discreet

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40
Q

3 Problems associated w/ Peripheral PCA syndromes

A
  1. Transiet Global Amnesia due to hippocampal lesion
  2. Alexia (unable to read) w/out agraphia (still able to write)
  3. Visual symptoms
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41
Q

What are the visual symptoms assoc’d w/ peripheral PCA syndrome

A

* cortical blindness—occ. lobe directly affected

* Homonymous hemianopsia–portion of vis. field missing

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42
Q

Vertebral Artery syndromes

Vertebral arteries FORM Basilar aa’s

Anterior BS

A

see pic

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43
Q

PRIMARY arterial supply to medulla, AND post, inf, Cb

A

Vertebral artery

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44
Q

what is the Vertebral artery the PRIMARY arterial supply to?

A

Medulla

Post, Inf Cb

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45
Q

Commonly occluded by atherosclerosis

susceptible to trauma (MVA), OR inappopriate EXT–rot. manipulations

*inapp. C-spine manips

A

Vertebral aa syndrome

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46
Q

MOST common cause vertebral artery syndromes

A

Atherosclerosis

also inappropriate manipulations of C/S

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47
Q

Well-documented in Wallenberg’s (Lat. Medulla) Syndrome

A

Vert. Artery syndrome

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48
Q

Lateral Medullary or

Wallenberg’s Syndrome

Think…

A

Vertebral artery syndrome

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49
Q

Lateral Medullary Syndrome

*Assoc’d w/ Vertebral artery syndrome

A
  • vertigo
  • nausea
  • hoarseness
  • dysphagia
  • Horner’s syndrome
  • ipsilateral ataxia
  • ipsilateral loss of facial sensation to pain and temp
  • ipsilateral loss of sensation on arm, trunk, leg
  • Contralateral loss of pain/temp in arm, trunk, leg
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50
Q

3 signs of Horner’s Syndrome

*Lat. Medullary Syndrome

A
  1. constricted pupil
  2. Ptosis (droopy eyelid)
  3. DEC sweating
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51
Q

IPSILATERAL losses assoc’d w/ Lat. Medullary Syndrome

A
  • IPSILATERAL
    • loss facial sensation to pain and temp
    • ataxia
    • loss of sensation arm, trunk, leg
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52
Q

CONTRALATERAL loss assoc’d w/ Lat. Medullary syndrome

A
  • CONTRALATERAL
    • loss of pain/temp arm, trunk, leg
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53
Q

Basilar Artery syndrome

*2 vert aa’s come together to form Basilar aa

Anterior BS

A

see pic

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54
Q

Basilar artery supplies Central areas:

what are they?

A
  1. PONS
  2. Superior cerebellar peduncles
  3. portions of Midbrain, Cb, diencephalon

*Central areas

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55
Q

Why can Basilar artery syndrome be catastrophic?

A

Pontine damage

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56
Q

Basilar aa syndrome can be catastrophic bc of the pontime damage

what happens as a result?

A
  • Tetraplegia
  • Coma
  • “Locked-in” Syndrome–> Trapped inside your own body
    • basically…
      • person FEELS conscious, oriented, alert
        • NO capacity for motor output
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57
Q

When Dr. Cohen says “Cerebellum”

you say…….

A

COORDINATION!!!!!!

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58
Q

Cb is supplied by 3 arteries

what are they?

A
  • 2 branches from Basilar aa
    • ​SCA
    • AICA
  • 1 branch from Vertebral artery
    • ​PICA
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59
Q

in GROSS terms….

what does the Cb do?

A

adds precision to mvmt control

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60
Q

very obvious that since the Cb adds precision to mvmt control that it must have a role in _________________ or ______________-

A

BALANCE

or maint. of postural stability

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61
Q

3 lobes of the Cb

A
  1. Anterior
  2. Middle
  3. Flocculonodular
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62
Q

Anterior lobe: Cb

A

Posture

Trunk mvmt

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63
Q

Middle lobe Cb

A

Coordination

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64
Q

Flocculonodular lobe Cb

A

Mm tone and Eye mvmt

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65
Q

How is the Cb connected to rest of the brain?

A

Cerebellar peduncles

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66
Q

Cb receives many ________ projections from the _____, ______, and ________ brain regions

A

AFFERENT

cord, cortex, subcortical brain reg’s

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67
Q

The Cb receives INPUT from motor and NON-motor areas

4 areas:

A
  1. somatosensory
  2. vestibular
  3. auditory
  4. visual
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68
Q

w/ connections to the Cb

afferents outnumber efferent 40:1

but extensive outgoing projections to 4 areas:

A
  1. cortex
  2. BS
  3. midbrain
  4. SC
69
Q

Cb promotes 3 things :

A
  1. synchrony
  2. accuracy
  3. Coordination
70
Q

Specifically when it comes to Cb and Coordination

Coordination of what?

A
  • Postural and Equilib responses
  • Voluntary and reflex mm actions
71
Q

Cb regulates mvmt via 3 systems

A
  1. Vestibulocerebellar system
  2. Spinocerebella
  3. Cerebrocerebellar
72
Q

Vestibulocerebellar system modifies what?

A

Vestibular influences on posture and eye mvmt

73
Q

Spinocerebellar system regulates:

A

Regulates mm tone, posture, locomotion

74
Q

Cerebrocerebellum regulates:

A

Skilled mvmt

75
Q

When you see Cb think……

A

COORDINATION!!!

76
Q

the Cb in regards to the enrichment of mvmt quality

regulatory center for control of this kind of activity and constructs normal what?

A

Reg. center for control of motor activity

participates in construction of normal synergies

aka Motor Skill learning

77
Q

Comparator of mvmt

78
Q

In regards to being a comparator of mvmt:

Cb compares what ?

A

Motor plan vs. execution===> compensates for errors

think of the grabbing carton of milk from fridge thinking it’s full but its actually empty

79
Q

How does the Cb “compare” mvmts

A

rec’s inputs from ALL lvls of CNS AND periphery

80
Q

Cb is involved in the ______, ________, and _______ of Muscle activation

A

Timing

Sequence

Scaling

81
Q

how does Cb regulate mvmt and posture ?

A

adjusts output of descending tracts

82
Q

Cb scales _______/_____ responses to meet task demands

A

muscle/synergy

83
Q

Cb’s role on modulating cord and BS influences

A

modulates cord/BS influences on posture and mvmt to stabilize during perturbations

Ex: walk to dry erase board and write a LARGE A and SMALL A

Lg. A uses more shoulder to draw, Sm. A uses more fingertips

Pattern execution similar but little different

Cb scales this mvmt

84
Q

Visual tracking effect of Cb

A
  • coordinates mvmts to track moving and stationary obj’s and to analyze sensory consequences
  • ***Problem here==> inability to perform a task in accordance w/ its spatial and temporal constraints
    • lack of hand-eye coord.
85
Q

W/ the Cb:

Lesions to the central anterior, posterior lobes and vermis:

results in:

A
  • LE dyscoordination
  • deficits in LE equilib responses
  • abnorm. head and trunk synergies occur
  • BASICALLY AN INABILITY TO BALANCE
86
Q

In relation to balance and equilibrium and the Cb

study of Posturography of pts w/ anterior Cb degen

showed what?

A
  • Normal response latencies—> time b/w stim and response
  • BUT….
  • amplitude and duration of these responses were 2-3x normal
  • no habituation to stimuli
    • no “getting used to it” or learning how to respond
  • characteristic 3Hz postural sway
    • ​much faster than normal indiv’s
87
Q

W/ Cb dysfunction and balance

this is enhanced

A

Intersegmental counterbalancing

*stiffer limbs==closed-pack pos.

LOWER-than-expected falls BUT stiff-legged gait

BOS widened to LOWER COG

88
Q

Tests that are POSITIVE w/ Cb dysf. and balance

A

+ Tandem walking test (heel-to-toe)

+ Heel to shin test—coord. test

*arm swing gen. absent

89
Q

regs. mm activity to compensate for changes in load during mvmt

A

Spinocerebellum

90
Q

Spinocerebellum regulates mm activity to compensate for what?

A

changes in load during mvmt

91
Q

The spinocerebellum regs mm activity to compensate for changes in load during mvmt

so basically it regulates these two things:

A
  1. tone
  2. force production

*interacts w/ spinal musculature

92
Q

Vestibulocerebellum aka

A

Vestibular control system

93
Q

Lesions here cause instability of head and trunk==> imbalance

A

vestbulocerebellum

94
Q

lesion to vestibulocerebellum causes instability of head and trunk==== imbalance

No ability to what ?

A

substitute w/ visual fixation

*similar to peripheral vestib. issues (inner ear)

95
Q

Sx included w/ vestibulocerebellum dysf.

A

Nausea

nystagmus

vertigo

vomiting

*not evident when body in SUPINE

96
Q

Where does the vestibulocerebellum receive INPUT from ?

A
  • FROM Vestibular system
    • CN VIII and vestib nuclei in BS
97
Q

Vestibulocerebellum OUTPUTS?

A

Vest. system

VOR or VSR

98
Q

VOR

A

Vestibular Ocular Reflex

fixes eyes as we move

to extra-oc mm’s

99
Q

VSR

A

Vestibular Spinal Reflex

posture

to spinal mm’s

100
Q

Assoc’d w/ refining mvmt & motor skill learning and prep.

A

Cerebrocerebellum

101
Q

Feed-forward/Anticipatory mechanisms

Think…..

A

Cerebrocerebellum

102
Q

Lesions to Cerebrocerebellum interfere w/ ______ and __________

A

Motor learning

prep for mvmt

103
Q

Cerebrocerebellum plays a MAJOR role in _________ of quick mvmts

A

Precision of quick mvmts

104
Q

What is the cerebrocerebellums major role in precision of quick mvmts ?

A

modulates agonist/antagonistic interactions

===> dexterity during manual tasks

105
Q

Timing of mvmt

Judging time and speed in perceptual-motor task

A

Cerebrocerebellum

106
Q

In general….

Role of Cb is to what?

A

Control details of the execution of a motor task

107
Q

Although the inititation of mvmt begins @ Cortical lvl….

Cb plays a role how?

A

task execution

spares us from having to THINK out EVERY mvmt

enables us to act AUTOMATICALLY

108
Q

Etiology of Cb damage: MOST COMMON CAUSE?

109
Q

Overall Etiology of Cb damage:

A
  • TBI–most common
  • developmental abnorm.
    • hypoxia
    • hydrocephalus
  • demyelinating dis’s—> MS​
  • hereditary dis.
  • Metabolic disorders
    • Wilson’s Dis.
  • Vascular insuff’s
  • Drug + alc. intoxications
110
Q

The effects of Cb lesions are…..

ipsi or contra???

A

IPSILATERAL!!!!

111
Q

For s/s Cb lesions to be noted…..

A

damage must be fairly extensive

*esp if degenerative

112
Q

Cb regulates vestibular, spinal, and cortical mech’s via:

A

Reciprocal connections

*afferent and efferent connections

(outputs and inputs)

113
Q

S/S Cb damage

A
  • ataxia
  • hypOtonia
  • dysarthria
  • asthenia
  • tremor
  • nystagmus
  • Gait and balance abnorms
114
Q

S/S of Cb damage: Ataxia

what can be included in this?

A
  • Ataxia
    • Dysmetria
      • inability to control distances, speed, ROM for smoothly coord’d mvmts
        • ​over-reaching
    • Dysdiadochokinesia
      • rapid mvmts (hands turning over)
    • Rebound/lack of check
    • Ataxic gait
115
Q

Cb damage: HypOtonia

A
  • loss of normal reinforcement to Cortical Motor Signs
  • MAX force OUTPUT un-impaired
    • ​ability to sustain force impaired
116
Q

Cb damage: Dysarthria

A
  • Poor coordination speech and breath support
    • ​scanning speech
    • spacing of sounds irregular w/ pauses in WRONG places
117
Q

Cb damage: Asthenia

A
  • MM weakness
    • lack of control and coord. of forces and timing of mm contraction
  • NOTE: Cb lesions DELAY mvmt initiation BUT do NOT prevent it like PD
118
Q

Cb damage: Gait/Balance abnorms

A
  • Midline lesion Cb=== deficits in maint upright stance
  • vis. input==little influence on cerebellar ataxia
  • staggering gait like someone who is drunk
119
Q

If a pt. has a (L) Cb pathology, eval reveals normal motor and sensory function

EXCEPT:

A
  • INC BOS during gait
  • veer to L during ambulation (esp w/ eyes closed)
  • unable to maint. unilateral stance L side
  • intention tremor in L UE
  • L extremity dysmetria and dysdiadochokinesia
120
Q

Cb damage can include vestibular s/s:

A
  • direction changing nystagmus
  • dizziness
  • nausea/vomiting

**Motion sickness sx’s

121
Q

Two other known Cb patho’s

A
  1. Friedrich’s Ataxia
  2. Chronic alcoholism and Wernicke-Korsakoff Syndrome
122
Q

Friedreich’s Ataxia

*wide variety of Cb dysf.*

A
  • INHERITED dis.
    • children 5-15yo
  • progressive damage to NS
    • ​degen of nerve tissue
  • 1 in 50,000 people US
  • Lifespan==30-40yrs after dx
123
Q

Chronic alcoholism may result in:

A

Wernicke-Korsakoff Syndrome

*Vit. B deficiency

124
Q

s/s Chronic alcoholism and Cb

A

ataxia

coma

confusion

125
Q

What should you remember about Hemorrhagic CVA?

A

LESS common

MORE fatal BUT….

if you recover the prognosis is BETTER vs. ischemic because ischemic leads to tissue destruction

126
Q

Hemorrhagic CVA: most common types

A
  • ICH (intra-cerebral)
    • due to HTN
  • Cerebral amyloid angiopathy
    • weak blood vessel walls
  • SAH (sub arachnoid)
    • due to ruptured saccular aneurysm
  • AVM
    • Arterial Venous Malformation
127
Q

Although there are MOST COMMON types of Hemorrhagic CVA

they can also be caused by these three things:

A
  1. Hyperanticoagulation
  2. Hemorrhage into brain tumor
  3. Trauma (TBI)
128
Q

MOST FATAL OF ALL CVA subtypes??????

129
Q

ICH is bleeding from where???

A

from arterial source INTO brain parenchyma

MOST FATAL OF ALL CVA SUBTYPES

130
Q

ICH broken down into:

A

Primary vs. Secondary

131
Q

Spontaneous bleed

usually due to microvascular disease assoc’d w/ HTN and/or Aging

A

Primary ICH

132
Q

Primary ICH

A

Spontaneous bleed

usually due to microvascular disease assoc’d w/ HTN and/or Aging

*small penetrating aa’s most freq. involved

133
Q

Secondary ICH occurs due to: 3

A
  1. toxic exposure
  2. impaired coagulation
  3. trauma
134
Q

SAH are hemorrhages into the ______________

A

SubArachnoid space

b/w Arachnoid and Pia mater ***

135
Q

SAH in NON-traumatic cases

most common types in these cases?

A

Aneurysms

Vascular formations

136
Q

What else could you possibly get SAH from ?

A

trauma

dev. defects

neoplasms

infection

137
Q

In normotensive persons….. these can spontaneously occur?

138
Q

SAH and Berry aneurysm

139
Q

90% of SAHs are due to this???

and WHERE do they occur ?

A

90% due to Saccular or berry aneurysms

occur @ bifurcations

140
Q

What is normally the stimulus for a SAH?

Cause?

A
  • Transient rise in BP
    • ​valsalve
    • intercourse
141
Q

There are 3 arteries that are the most common sites for SAH

A
  1. Ant. communicating aa
  2. Post communicating aa
  3. MCA
142
Q

Dangers of SAH

A
  • spewing of blood==high pressure==into brain tissue
  • susceptible to re-rupture
  • obstruction of SA space
    • ​—> hydrocephalus due to CSF blockage
143
Q

In an SAH, the obstruction of the SA space leads to what?

A

Hydrocephalus due to CSF blockage

144
Q

Regarding dangers to SAH, now there is blood in the SA space

this will lead to 2 things:

A
  1. vasospasm
  2. inflamm and fibrotic responses in meninges

2* comps are often fatal

145
Q

Vasospasm from blood in the SA space ===>

A

ischemic infarction of adj. vessels

146
Q

In SAH

the hemorrhage causes extreme INC in ICP

why is this?

A

Obstructed CSF coupled w/ brain edema

147
Q

Lethal brain herniations, which is crushing of the brain tissue AGAINST bony surfaces occurs as result of?

A

occur as result of INC pressure and mass w/in cranial cavity

Primary sites==> bones of orbit OR post. fossa

148
Q

SAH: Mild to Severe

Explain MILD

A

Stiff neck

mild HA

min. focal neuro. signs and confusion lasting for weeks

149
Q

SAH: Moderate

A

mild coma

mod-severe HA

*sig. chance rebleeding

150
Q

SAH: Severe

A

can be fatal

severe HA

Decerebrate rigidity (extension, one w/ all the e’s)

deep coma

*sig. chance of rebleeding

151
Q

AVM: Atriovenous Malformation

A

Big tangle of aa’s and veins

see pic

152
Q

WHO do AVMs occur in mostly?

A

YOUNGER PEOPLE

20-30yo

153
Q

Size AVM?

A

Tiny all the way to the size of a whole hemisphere

154
Q

AVM appearance?

*just think of a big tangled mess of aa’s and veins

A
  • Tangle of aa’s and veins
  • persistence of an embryonic pattern of blood vessels
155
Q

AVM is the result of abnormal_______________

A

abnormal fetal development

156
Q

Smaller AVMs vs. Larger AVMs

and other facts

A
  • 1-4% risk of bleed
    • preceded by HA + seizures
  • Smaller==MORE likely to bleed
    • due to elevated arterial press in smaller vessels
  • Larger==LESS likely to bleed
157
Q

AVM hemorrhages can either be _______ or ________

A

Parenchytamous

Subarachnoid

158
Q

Why are bleeds less devastating w/ AVMs?

A
  • LESS devastating bc the bleeds primarily into the malformation only
    • ​ only incidentally into the adjacent brain
      • NOTE: brain tissue supplied by the AVM is NON-functional (never had blood supply so cannot be damaged)
159
Q

LT prognosis for AVM

A

GOOD

90% survive first bleed

160
Q

Syndromes assoc’d w/ Hemorrhagic CVA tend to be LESS FOCAL vs. Ischemic

Why is this?

A

more generalized area of tissue involve.

remember ischemic can be in one spot and completely destroy that spot

161
Q

This particular hemorrhage is similar to MCA CVA, but w/ greater alteration of consciousness

A

Putaminal hemorrhage

162
Q

Putaminal hemorrhage think…..

A

similar to MCA CVA

GREATER alteration of consciousness

163
Q

4 syndromes assoc’d w/ Hemorrhagic CVA

A
  1. Putaminal hemorrhage
  2. Thalamic hemorrhage
  3. Cerebellar hemorrhage
  4. Pontine hemorrhage
164
Q

Thalamic hemorrhage

A
  • Contralateral hemiplegia
  • disproportionately greater sensory loss

W/ thalamus—> greater sensory loss

165
Q

Cerebellar hemorrhage

A

ataxia

vestibulopathy

166
Q

Pontine hemorrhage

@PONS

A

POOREST PROGNOSIS

Tetraplegia + coma

many paths affected + sleep/wake cycles

167
Q

MORE deadly, but BETTER prognosis w/ recovery

A

Hemorrhagic CVA

bc compression NOT destruction

168
Q

LESS freq’ly fatal, but POORER prognosis for functional recovery

A

Ischemic CVA

bc damage caused by ischemia DIRECTLY

169
Q

Hemorrhagic vs. Ischemic

prognosis and recovery differences:

A
  • Hemmorhagic CVA:
    • more deadly, but better prognosis for recovery
    • compression, NOT destruction
  • Ischemic CVA:
    • less freq’ly fatal, but poorer prognosis for functional recovery
    • caused by ischemia directly

MedCon Rehab II (5 decks)

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